Tài liệu tâm lý học sức khỏe: Ảnh hưởng của văn hóa xã hội đối với tâm lý sức khỏe

24
Sociocultural Influences on Health
Caroline A. Macera
Centers for Disease Control and
Prevention
Cheryl A. Armstead
University of South Carolina
Norman B. Anderson
National Institutes of Health
The health experience of Americans has improved enormously over the
course of the 20th century. Communicable and infectious diseases, the
major causes of premature death in the United States prior to 1930, have
been replaced by chronic illnesses such as heart disease and cancer.
Furthermore, age-adjusted mortality from heart disease has decreased from
307.2 per 100, 000 in 1950 to 138.3 per 100, 000 in 1995. Similarly, infant
mortality has decreased from 12.6 per 1, 000 live births in 1980 to 7.6 per 1,
000 live births in 1995. These changes mean that a majority of people in this
country can expect to live a long and productive life. In fact, a child born in
1995 could expect to live 75.8 years compared to 47.3 years for a child born
in 1900 (National Center for Health Statistics, 1997).
Unfortunately, these astounding improvements in health status have not
affected all Americans equally. Lagging behind are many of the underserved
and minority populations (Kington & Smith, 1997; Liao & Cooper, 1995). The
ethnic composition of the U.S. population has changed from being primarily
White to include a large percentage of African Americans (or Blacks),
Hispanics, and Asian and Pacific Islanders. This cultural diversity will
continue to increase because of high immigration and birth rates among
minority populations. Each ethnic group views health within its own cultural
context, which complicates the decision to seek and continue treatment, and
to use preventive measures. Additionally, social conditions may put
minorities at higher risk for specific health problems. The purpose of this

chapter is to first present basic demographic and health characteristics of
the major ethnic groups in this country, and then to describe a contextual
model of hypertension in Blacks as an example of how ethnic disparities in
health status may occur and be understood.

DISTRIBUTION OF ETHNIC MINORITIES
Although there is a great deal of diversity within ethnic groups, this chapter
uses the five general categories as collected and reported by the National
Center for Health Statistics (1997): White, Black, American Indian or Native
Alaskan, Asian and Pacific Islander, and Hispanic origin. When possible, data
is presented by non-Hispanic White and non-Hispanic Black groups. Because
there is no consistent agreement on terminology, this chapter uses African
American and Black interchangeably throughout.
African Americans, or Blacks, the largest minority group in the United States,
number almost 34 million and represent 12.8% of the population (U.S.
Bureau of the Census, 1995). During 1994, the African American population
grew at a faster rate than the White population (1.5% compared to only


0.8%), but not as fast as the Hispanic population (3.5%). Blacks are
projected to be the second largest minority group in this country by 2025 (
Fig. 24.1 ).
-427FIG. 24.1
The term Hispanic is used to summarize information about people of all
races whose ancestry can be traced to Spain, Mexico, Puerto Rico, Cuba, or
to any of the Spanish-speaking Latin American countries. The 1990 census
enumerated 29.2 million Hispanics classified as Mexican Americans, Puerto
Ricans, Cuban Americans, and about 30 additional Hispanic- origin groups
aggregated as Other Hispanics (U.S. Bureau of the Census, 1995). Hispanics
in the United States represent about 10.9% of the population and are the

nation's second largest minority group. However, because of high
immigration and birth rates, Hispanics are expected to replace American
Americans as the largest ethnic minority group in the United States by 2025.
Asians and Pacific Islanders in the United States number about 10 million
(representing 3.7% of the population), and speak more than 30 major
languages or dialects (U.S. Bureau of the Census, 1995). The major groups in
this category include Chinese, Filipinos, Japanese, Koreans, and Native
Hawaiians. Furthermore, about two thirds of the persons in this population
group speak their native language at home, and more than 60% of
Southeast Asians (Vietnamese, Cambodian, Hmong, and Laotian) have
limited proficiency in English. Although a small proportion of the U.S.
population, this diverse minority group is expected to increase to more than
five times its current size and represent 10.3% of the population by 2050
(US. Bureau of the Census, 1995).
Native Americans in the United States number about 2.3 million, just less
than 1% of the population. Although this group is expected to grow steadily
over the next 50 years, the percent of the population that is American Indian
or Alaskan Native would only rise to 1.1% by 2050, remaining the smallest
minority group in the United States (U.S. Bureau of the Census, 1995).

LIFE EXPECTANCY
One measure of the health of a population is its life expectancy, a value that
heavily weights early morality, but does not incorporate quality of life issues.
Throughout the 20th century, African Americans experienced substantial
improvements in life expectancy, but they still have an estimated life span
of 6 to 8 years less than Whites (Table 24.1). For both Whites and Afican
Americans, women live longer than men, resulting in a higher proportion of
women alive, especially in the older age groups. The life expectancy at birth
for African American men increased 2.2% (or 1.4 years) from 1980 to 1995
compared to a 38% (or 2.7 years) increase for White men. The increase in

life expectancy for African American women during this same period was
identical to that for White women, 1.9% (about 1.5 years; National Center
for Health Statistics, 1997).
Although comparable national data are not available for the other ethnic
groups, information on residents of Texas suggests that life expantancy at
birth for Hispanics is the same as non-Hispanic Whites and higher than non-


Hispanic Blacks (Centers for Disease Control and Prevention, 1994;
Markides, 1989). Similarly, area-specific studies have found life expectancy
for Asian and Pacific Islanders in the United States to be higher than that of
Whites. However, data on life expectancy for Asians may be particularly
subject to
-428-

misclassification and underestimates of the number of deaths within ethnic
groups (Gardner, 1994; Hahn, Truman, & Barker, 1996).
Life expectancy for Native Americans is lower than for Whites primarily
because of the high death rate for persons under age 45. This higher rate is
due to excess mortality from intentional and unintentional injuries rather
than from chronic diseases. The death rates for Native Americans are based
on death certificate identification of the decedent as a member of this
minority group. Unfortunately, it has been demonstrated that many Native
Americans have been classified as White on death certificates (Classification
of American Indian race on birth and death certificates, 1993; Frost, Taylor, &
Fries, 1992; Hahn et al., 1996; Sugarman $I Lawson, 1993), thereby
artificially reducing the death rate for persons in this group.

MAJOR CAUSES OF DEATH
As shown in Table 24.2, the highest death rate in 1995 is found for Black

men (1, 016.7 per 100, 000). Although most men and women in all ethnic
groups experienced a decline in overall mortality rate from 1985 to 1995,
the largest decline was among White men (9.6%). Ethnic differences are
apparent for mortality, but also for other health indicators such as
preventable hospitalizations (Pappas, Hadden, Kozak, & Fisher, 1997).
By examining the top five causes of death (Table 24.3), it is clear that all
ethnic groups share some common characteristics in spite of the differences
in mortality rates. Among the leading causes of death for both men and
women in most ethnic groups are diseases of the heart and cerebrovascular
disease (stroke). A major chronic condition associated with these conditions
is hypertension. After heart disease and stroke, the major contributors to the
high mortality rate among Black men are HIV infection, violence, and
unintentional injuries.

HEALTH STATUS
Unlike identifying the major causes of death, measuring good health is a
complicated task. Often health status is simply defined as the absence of
disease, even though a complex of physical, social, cognitive, and
psychological factors are involved in determining overall health. This chapter
uses high blood pressure, or hypertension, as a marker for health status
because of its association with the major causes of death and disability for
all ethnic groups. Hypertension is usually defined as having a systolic
pressure of at least 140 mm Hg or a diastolic pressure of at least 90 mm Hg,
or taking antihypertensive medication. About half the people who have
hypertension are undiagnosed. Furthermore, only about one fourth of those


who know they have the disease have controlled through lifestyle
modification or medication (Havas et al., 1996). Uncontrolled hypertension
increases the risk of circulatory diseases (particularly heart disease and

stroke), and kidney disease (Burt et al., 1995).
Because it is an important marker of health, questions about hypertension
are routinely included in national surveys, thus providing comparable
estimates of the prevalence of hypertension for White, African American,
and Mexican American subgroups. As shown in Fig. 24.2 and Table 24.4,
African Americans have the highest prevalence of hypertension, almost 1.5
times that of Whites, whereas Mexican Americans have an intermediary
prevalence (Burt et al., 1995; National Center for Health Statistics, 1997).
The percentage of the population with hypertension has decreased between
1976 and 1980 and 1988 and 1994 for Whites and African Americans, but
has remained constant for Mexican Americans: The decrease was over 40%
among Whites, but less than 30% among Blacks. Consequently, Blacks will
continue to experience disproportionately higher rates of morbidity and
mortality from heart disease, stroke, and renal disease compared to the
other ethnic groups.

-429-

FIG. 24.2. Percent of population with hypertension among persons from age
20 to 74, in the United States from 1976 to 1980 and 1988 to 1994.
(Hypertension is defined as either systolic pressure of at least 140 mm Hg or
diastolic pressure of at least 90 mm Hg, or taking antihypertensive
medication.) From National Center for Health Statistics (1997).
-430-

For less than 10% of those with hypertension, there is a definite cause.
However, for over 90% of people with hypertension, the cause is unknown
and it is termed essential hypertension (Frohlich, 1994). Hypertension occurs
more frequently among Blacks, older individuals, less educated individuals,
those who are obese or have gained weight, those who are physically

inactive, and those who use alcohol excessively. Additionally, some
individuals with augmented sodium metabolism may develop hypertension
(Frohlich, 1994). Because none of these risk factors alone explains a majority
of the risk for developing hypertension, it is clear that this disease develops
from multiple interacting mechanisms rather than from a single source
(Calhoun & Oparil, 1995; Flack et al., 1995). Among the contributors to this
disorder are genetic, biological, nutritional, behavioral, social,
environmental, and psychological factors.

SOCIAL AND CULTURAL FACTORS
RELATED TO HEALTH STATUS
Given the changing demographic makeup of the United States, it is
necessary to examine subpopulations within the major ethnic groups that


may be at high risk for disease. The rest of this chapter focuses on the
development and description of a model that may explain how social and
cultural influences interact to affect health status, using the example of
hypertension in Blacks. Although this model focuses on Black/White
differences in hypertension risk, many elements of the model may be
generalizable to other ethnic subpopulations and other health problems.

Contextual Model of Hypertension in
Blacks
The contextual model of hypertension in Blacks reflects the contribution of
sociology, psychology, and the natural sciences in attempting to
systematically understand the key determinants of ethnic differences in the
development and maintenance of hypertension. The unacceptableness of
unidimen sional or strictly genetic accounts of the determinants of
hypertension in Blacks is exemplified in the Report of the Secretary's Task

Force on Blacks and Minority Health (1986):
Black, in the United States is a sociological category. Some investigators
have confused ethnic identity with genetic constitution, simplistically
equating them. The heterogeneity of blood pressure levels and hypertension
prevalence in Black populations in Africa, the Caribbean, and the Americas
casts doubt on the proposition that genetic factors are primarily responsible
for the blood pressure excess in U.S. Blacks. …It becomes clear that any
explanation of blood pressure differences between Black populations must
take into explicitly account of environmental
Within the contextual model, hypertension risk factors interact with ethnicity
in the context of the environment and culture.

Cardiovascular Reactivity
In recent years, researchers in health psychology and behavioral medicine
have explored the role of cardiovascular reactivity as a potential contributor
to the high rates of hypertension. Reactivity is defined as the magnitude and
pattern of acute changes in cardiovascular activity (reactivity) in response to
behavioral, social, and environmental stressors. According to Krantz and
Manuck (1984), the measurement of reactivity contributes unique
information regarding the physiological functioning of the individual beyond
that provided by resting or baseline levels alone. The reactivity hypothesis
rests on the assumption that acute changes in cardiovascular reactivity to
laboratory procedures are analogous to cardiovascular challenges
encountered in daily life (Anderson, McNeilly, Armstead, Clark, & Pieper,
1993). Reactivity studies also suggest that exaggerated changes in
cardiovascular parameters, which occur when individuals are exposed to
behavioral, psychological, or physical challenges precede the development
of sustained hypertension (Julius & Schork, 197 I). Individuals at risk for
hypertension show greater sympathetic nervous system reactivity to
stressors. In animal as well as human research, groups at risk for

hypertension have shown greater stress reactivity than groups with
relatively lower risk. For example, “hyperreactivity” has been observed in
Blacks as compared to Whites, in anxious versus nonanxious persons, in
anger suppressors versus anger expressors, and in chronically stressed
versus nonstressed individuals. Hyperreactivity is thought to be a risk
marker for hypertensive risk and may be also directly implicated in the


pathogenesis of hypertension.
There have been a substantial number of studies on Black- White differences
in autonomic reactivity (Anderson, McNeilly, & Myers, 1992). These studies
have been conducted with both children (Dysart, Treiber, Pflieger, Davis, &
Strong, 1994; Murphy, Stoney, Alpert, & Walker, 1995) and adults (Anderson,
1989) and have utilized a wide variety of laboratory
-431stressors, experimental designs, physiological measures, and population
subgroups. Despite the diversity of approaches used, most studies have
demonstrated that Blacks show a greater blood pressure reactivity to
laboratory stressors as compared to Whites. Perhaps more important, is that
the mechanisms responsible for producing the stress-induced blood pressure
response may be different in Blacks than in Whites. Blacks have been found
to exhibit greater blood pressure reactivity mediated by peripheral
vasoconstriction (characteristic of the vascular pattern of reactivity; Girdler,
Hinderliter, & Light, 1993; Terrell & Manuck, 1996), whereas the blood
pressure response of Whites has shown a greater cardiac involvement
(characteristic of the cardiac pattern of reactivity). These results, particularly
the heightened peripheral vasoconstrictive responses in Blacks, have been
observed among children, adults, normotensives, and borderline
hypertensives. It has been most clearly seen in studies using stressors, such
as the forehead cold pressor test, that are specifically designed to produce a
predominantly vascular pattern of reactivity among Blacks. The studies have

not consistently found greater reactivity in Black adults with a positive
family history (Anderson, Lane, Taguchi, & Williams, 1989; Anderson, Lane,
Taguchi, Williams, & Houseworth, 1989).

Augmented Reactivity in Blacks
Thus far, research using the reactivity paradigm has been largely concerned
with describing racial differences in reactivity. The next logical step is to
identify the variables that are predictive of heightened vascular reactivity
among Blacks. Anderson et al. (1991) noted that physiological and
psychophysiological responses obtained in an experimental laboratory are
partly a function of the socioecological niche that the individual occupies at
that time.
The principal tenet of the proposed contextual model is that the
exaggerated peripheral vascular reactivity observed in many Blacks relative
to Whites is a function of a number of biological, psychological, behavioral,
environmental, and sociocultural factors. The model begins with the premise
that in reactivity research, race should be viewed as a proxy for the effects
of differential exposure to chronic social and environmental stressors rather
than as a proxy for the effects of genetic differences. Black Americans, on
average, are exposed to a wider array of chronic stressors than their White
counterparts. These chronic stressors interact with nervous system activity,
which in turn leads to the release of neuroendocrine substances, including
norepinephrine and adrenocorticotrophin hormone (ACTH), augmented
sodium retention, and enhanced vasoconstriction. The resulting higher levels
of endogenous sodium and ACTH not only increase blood volume but also
act to potentiate the vasoconstrictive effects of norepinephrine on the
peripheral vasculature. Over time, the repeated stressor- induced episodes
of vascular reactivity may lead to structural changes in the vascular wall
(e.g., increased wall-to-lumen ratio), which further augments reactivity. If
repeated frequently over a number of years, this process has the potential to

lead to the development of sustained hypertension. The remainder of this
chapter is devoted to describing each component of this model.

Chronic Stressors and the Social
Environment
Many writers view race as a sociological designation that indicates exposure
to common life experiences. According to the model presented here, one
distinguishing feature of the life experiences between Black and White
Americans is exposure to chronic life stressors. As a consequence of
historical factors and the continued race consciousness of society, Blacks
currently experience a greater array of chronic stressors relative to Whites.
These chronic socioecological stressors include, among others, higher
unemployment, higher poverty rates and lower income levels, lower status
occupations and lower social status, residential crowding, and substandard
housing (Bullard, 1994; Farley, 1984; Farley & Allen, 1989; Harris, 1982;
McLoyd, 1990). Many of these chronic social and environmental stressors
have been associated with hypertensive status among Blacks. For example,
socioeconomic status shows a strong inverse relation with hypertension
among Blacks (Adams-Campbell, Brambilla, & Minlay, 1993).
Racial Stress. Racism represents one of the most pernicious forms of chronic
psychosocial stress facing African Americans today. A burgeoning body of
literature identifies racism as a macrosocial factor contributing to the vast
racial disparity of health outcomes found among African Americans and
Whites (Jackson et al., 1996; McNeilly et al., 1996). Racial stress has been
found to be related to both blood pressure status (Krieger, 1990; Krieger &
Sidney, 1996) and cardiovascular reactivity (Armstead, 1991; Armstead, K.
A. Lawler, Gorden, Cross, & Gibbons, 1989; Jones, Harrell, Morris-Prather,
Thomas, & Omowale, 1996; McNeilly et al., 1995; Morris-Prather et al.,

1996).
Historically, African Americans often received severe punitive sanctions for
expressing emotions they experienced when exposed to racism. Anger
suppression may be a historical coping style that presently serves as a
moderator of the interaction between racism and blood pressure status and
reactivity. Gentry, Chesney, Gary, Hall, and Harburg (1982) found that males
who are high in interracial hostility and who tend to keep anger suppressed
have the highest mean diastolic pressure. Krieger (1990) found that Black
women who reported usually accepting and keeping quite about racist
treatment were 4.4 times more likely to report being hypertensive than were
Blacks who talked to others. Among Whites, this relation did not hold true. In
another study, Krieger and Sidney (1996) found that hypertension was
significantly higher among working-class Blacks reporting that they typically
“accepted” unfair treatment and had not experienced racial discrimination in
one of seven situations relative to those reporting that they “challenged”
unfair treatment and experienced racial discrimination. Among professional
Black adults, systolic blood pressure was 9 to 10 mm Hg higher among those
reporting a higher frequency of discrimination
-432and those reporting that they “accepted” unfair treatment. Black-White
differences in blood pressure were partially explained by incorporating
variables for exposure and coping styles utilized with racial discrimination.


Armstead (1991) and Armstead et al. (1989) found that anger suppression
was related to increased diastolic reactivity to racist stimuli and to a speech
stressor. Vascular activation may be end products of chronic anger
suppression as a result of coping with racism. Chronic exposure to racial
stress may contribute to concomitant changes in the peripheral vasculature
in ways similar to other chronic stressors. Anger kinetics may play a role in
catecholamine release and subsequent hemodynamic changes associated

with racial laboratory stressors.
Lower Socioeconomic Status. The health history of African Americans in the
United States is filled with accounts of pervasive disease morbidity and
mortality associated with social stratification (Anderson & Armstead, 1995).
In U.S. society, social stratification occurs as a function of ethnicity, gender,
or socioeconomic status. The term socioeconomic status (SES) is typically
used to describe stratified inequality in ranking that exists in society.
Educational attainment is also one of the strongest predictors of health
outcomes in the United States. Higher educational attainment does not
consistently bring comparable health benefits for minorities (Pappas, Queen,
Hadden, & Fisher, 1993). For example, Blacks have significantly lower SES
than Whites by every measure. What is often not recognized, however, is
that at most levels of SES, morbidity and mortality rates are higher for
Blacks than for Whites (Lillie-Blanton & Laveist, 1996; Williams, 1996).
At present, it is unclear how SES differentially influences hypertension risk
behaviors or blood pressure-related knowledge, attitudes, and beliefs of
minorities. Stratification and discrimination may directly and/or indirectly
interact with socioeconomic status to create a highly vulnerable underclass
of African American citizens with poorer overall health, poorer health
behaviors, increased daily life stress, and lack of access to health care
(Williams, 1992). Lower SES Blacks may not only receive more exposure to
environmental risk factors, psychosocial risk factors, and deficits in medical
care, but also may be more vulnerable to them. Dressler (1996) found
diastolic blood pressure levels were associated with an interaction between
lower socioeconomic status and increased exposure to stressful life events.
In the case of essential hypertension, a consistently strong gradient for SES
exists, especially for African Americans. Among both Blacks and Whites,
hypertension is higher at the lower end of the SES spectrum, yet the relation
clearly reflects an interaction of gender, ethnic, and socioeconomic
stratification (Adams-Campbell et al., 1993; Williams, 1992).

If SES is linked to hypertension in a causative way, it should be expected
that it is also linked to physiological systems relevant to hypertension. One
possible biological mediator of SES effects on hypertension effect is
cardiovascular reactivity. Carroll, Davey-Smith, Sheffield, Shipley, and
Marmot (1997) examined the relation of SES, hostility, and blood pressure
reactions to mental stress in British men. They found that systolic pressure
reactivity was positively associated with SES. Higher SES was associated
with greater reactivity. Armstead, Anderson, and Lawler (1994) found an
interaction between SES and ethnicity for laboratory reactivity to a speech
stressor among African American and White women. Lower socioeconomic
status Black women demonstrated greater reactivity than White women or
higher SES Black women. This indicates that being Black and poor may
physiologically predispose individuals to hyperreactivity, which may be a risk
marker for essential hypertension.
SES is related to several factors known to enhance reactivity, such as
emotional suppression (Armstead et al., 1989; Durel et al., 1989; Johnson,


1989), lower levels of social support (Kamarck, Manuck, & Jennings, 1990),
and greater exposure to chronic stress (James & Kleinbaum, 1976). The
contextual model of hypertension suggests that lower SES may be an index
of exposure to these reactivity-enhancing factors, especially among Blacks,
and may serve as a predictor of augmented cardiovascular responsivity in
this group. If SES is related to reactivity, then ethnic group differences in SES
might partially account for the mixed reactivity results among African
Americans and Whites. Calhoun, Mutinga, Wyss, and Oparil (1994) suggest
that SES-related stress may cause sympathetic nervous system
hyperreactivity by vascular mechanisms.
Socioecological Stressors. Harburg et al. (1973) found that Detroit Blacks
residing in neighborhoods high in socioecologic stress, characterized by low

SES and high social instability (SIS; defined as high crime and divorce rates),
exhibited significantly higher blood pressures than Blacks living in low SES
but more stable neighborhoods. Among Whites, socioecologic stress did not
influence blood pressure.
Similarly, James and Kleinbaum (1976) found that for Black men from age 45
to 54, high stress counties (low SES, high SIS) of North Carolina were
associated with significantly higher hypertension- related mortality (e.g.,
hypertensive heart disease and stroke) than low stress counties. As in
Harburg's Detroit studies, no stress-mortality relation was found for White
men. In a study of residential crowding, Fleming, Baum, and Weiss (1987)
found that individuals living in densely populated neighborhoods had higher
blood pressure and greater heart rate reactivity during a challenging
behavioral task than those who lived in less crowded neighborhoods.
Family environment is a socioecological stressor that has been found to
influence hemodynamic reactivity in children prospectively (Wright et al.,
1993). For example, parental reports of greater conflict and control were
associated with vascular reactivity among 6- to 8-year-old children at a 2year follow-up. Thus, not only are Blacks exposed more frequently to chronic
stressors, but these socioenvironmental factors may have greater health
consequences for Blacks.

Chronic Stress and Vascular
Reactivity:
Physiologic Mediators
If the differential exposure to chronic stressors is related to acute
cardiovascular reactivity as proposed, it should be possible
-433to identify specific physiological mechanisms linking these phenomena in
Blacks. It is proposed that exposure to chronic stressors enhances
sympathetic nervous system activity that results in augmented sodium
retention and catecholamine release. Augmented sodium retention and
catecholamine release may, in addition to increasing blood volume,

contribute to the greater vascular responses in Blacks.
Sympathetic Nervous System (SNS) Effects. Of critical importance is whether
exposure to chronic stress is associated with this hypothesized physiological


scenario. In support of this, research from animal and human studies has
demonstrated that exposure to acute and chronic uncontrollable stress may
augment resting SNS tone; enhance sympathetic reactivity to acute, novel
stressors; elevate plasma levels of catecholamines, ACTH, and opioid
peptides; and augment sodium retention (Baum, Gatchel, & Schaeffer, 1983;
Davidson, Fleming, & Baum, 1987; Fleming, Baum, Davidson, Rectanus, &
McArdle, 1987; Koepke & DiBona, 1985; Koepke, Light, & Obrist, 1983; J. E.
Lawler, Naylor, & Abel, 1993; Lawler, Zheng, Li, Wang, & Edgemon, 1996;
Light, Koepke, Obrist, & Willis, 1983; McCarty, Horwatt, & Konarska, 1988).
Studies of reactivity indicate that norepinephrine elicits elevations in blood
pressure through vasoconstrictive effects on the peripheral vasculature
(Goldstein, 1983). ACTH has been shown to potentiate norepinephrine's
vasoconstrictive effects, particularly in humans and animals with reduced
renal excretory capacity (Bassett, Strand, & Cairncross, 1978; Strand Jz
Smith, 1980; Whitworth, Coghlan, Denton, Hardy, & Scoggins, 1979), and to
augment norepinephrine-induced contractions of a striated muscle (Bassett
et al., 1978; Strand & Smith, 1980). Importantly, ACTH also induces sodium
and water retention (Lohmeier & Caroll, 1985).
In a series of studies at the University of North Carolina and the University of
Iowa, investigators examined the role of stress and sodium retention in dogs
and spontaneously hypertensive rats (Grignolo, Koepke, & Obrist, 1982;
Koepke & DiBona, 1985; Koepke et al., 1983; Light, 1987). In these studies,
animals who were exposed to chronic stress showed significant reductions in
sodium and fluid excretion and an associated rise in blood pressure that was
mediated by renal sympathetic nerves. In perhaps the first study of stress

and sodium retention in humans, Light et al. (1983) discovered that a
stressful laboratory task (competitive reaction time) led to decreased urinary
sodium excretion in men with risk factors for hypertension (positive parental
history of hypertension and/or borderline hypertension) but only if these
men showed evidence of high SNS activity as indicated by above average
heart rate increases. It has also been found that low intake of dietary
potassium enhances vasopressor responses to cold stress in African
Americans, but not in Whites (Sudhir et al., 1997). Ionic mediation of
reactivity by sodium, calcium, and potassium interactions is implicated, but
remains largely unstudied.
Sodium Effects. sodium as a principal physiological mediator of heightened
vascular reactivity in Blacks. First, considerable evidence exists that
heightened sympathetic activity may induce sodium retention (Weinberger,
Luft, & Henry, 1982). Although the dietary sodium intake of Blacks may not
be significantly higher than that of Whites (Grim et al., 1980), Blacks excrete
less sodium in urine and exhibit greater pressor response to sodium loading
(Luft et al., 1979; Luft, Grim, & Weinberger, 1985). Thus, Blacks may be
more susceptible to the blood pressure effects of sodium despite a similar
dietary intake relative to Whites. Research suggests that sodium may
augment cardiovascular reactivity in subjects at risk for hypertension
(Ambrosioni et al., 1982; Ambrosioni, Costa, Montebugnoli, Borghi, &
Magnani, 1981; Falkner, Onesti, & Angelakos, 1981). Finally, studies in both
humans and spontaneously hypertensive rats indicate that sodium may
exert its influence on blood pressure via heightened vasoconstriction rather
than by increasing cardiac output (Nilsson, Ely, Friberg, Kalstrom, & Folkow,
1985). Therefore, given the influence of the SNS on sodium retention, the
greater sodium sensitivity among Blacks, and the effects of sodium on both
reactivity and vascular resistance, sodium may be the pivotal physiological
mechanism responsible for the observed race differences in vascular

reactivity.
How might sodium contribute to increased vascular resistance? Sodium may
lead to heightened vascular resistance through its effects on plasma
norepinephrine release and action. Although in normotensive individuals
sodium loading has been shown to decrease plasma and urinary
norepinephrine levels, the opposite effect has been observed for saltsensitive and hypertensive individuals. In these individuals, sodium loading
increases plasma and urinary norepinephrine levels, whereas sodium
deprivation has the opposite effect (Koolen & Van Brummelen, 1984; Luft et
al., 1979; Takeshita, Imaizumi, Ashihara, & Nakamura, 1982). Furthermore,
high sodium intake has been shown to potentiate the effects of
norepinephrine on the vasculature (Rankin, Luft, Henry, Gibbs, &
Weinberger, 1981), and has also been associated with increased pressor
responses to infused norepinephrine in Black hypertensives relative to White
hypertensives (Dimsdale, Graham, Ziegler, Zusman, & Berry, 1987). Thus, if
Blacks exhibit an exaggerated antinatriuresis, this may lead to an increased
release vasoconstrictive action of plasma norepinephrine. This chain of
events would increase peripheral vascular resistance in Blacks. Moreover,
chronic stressors that stimulate the release of plasma norepinephrine would
interact with higher prevailing sodium levels to further stimulate vascular
reactivity (Henry, 1988). Deter et al. (1997) found that salt sensitivity was
related to increased anger irritation levels and increased reactivity to an
information-processing task. They suggested that salt sensitivity,
psychosocial, and psychophysiological traits, such as reactivity, interact to
play a role in the pathogenesis of hypertension. It is hypothesized that the
heightened vascular reactivity observed in Blacks may ultimately result in
structural changes (i.e., hypertrophy) in the peripheral vasculature, which in
turn may further augment vascular hyperactivity (Folkow, 1982, 1987). A
long-term consequence of this process could be sustained hypertension.
-434In summary, compelling evidence exists that Blacks in American society are

systematically exposed to a wider array of chronic social stressors compared
to their White counterparts. These stressors involve lower SES, higher rates
of poverty, higher unemployment, lower status occupations, exposure to
racism, and more crowded and ecologically stressful residential
environments. Many have been related to elevated blood pressure and
increased hypertension prevalence. Research with humans and animals
suggests that exposure to chronic stress may increase tonic SNS activity,
acute autonomic reactivity, and urinary sodium retention. Future studies
may determine whether the types of stressors that many Blacks are exposed
to on a daily basis are related to these potentially pathological sequelae.

Bheamoral and Psychological
Factors
It is conceivable that chronic social stressors may increase catecholamine
release and sodium retention through specific behavioral or psychological
factors. Early research demonstrated an association between, anger, Type A
behavior, and higher levels of plasma norepinephrine and blood pressure
among Whites (Friedman, Byers, Diamant, & Rosenman, 1975). To date, only
one study has examined these relations in Blacks (Durel et al., 1989).
Although this study yielded nonsignificant relations between norepinephrine
and anger for both Blacks and Whites, it did demonstrate positive
correlations between anger and cardiovascular reactivity in these


individuals.
Several studies have shown that behavioral and psychological factors are
linked to elevated blood pressure and hypertension among Blacks
(Anderson, Myers, Pickering, & Jackson, 1989; James, 1985). For example,
suppressed anger and hostility have been associated with elevated blood
pressure and hypertension in both adolescents and adults (Harburg,

Blakelock, & Roeper, 1979; Johnson, Schork, & Spielberger, 1987; Johnson,
Spielberger, Worden, & Jacobs, 1987). In general, this literature has
indicated that Blacks who frequently suppress their anger when provoked, or
who express their anger without reflection, have higher resting blood
pressure levels than those who routinely express their anger when provoked
or who express it only after some reflection (Gentry et al., 1982). Recently,
the experience of frequent anger has been related to higher ambulatory
blood pressures among Black women while at work (Durel et al., 1989). At
this time, research has not examined whether inhibited anger expression is
related to sodium excretion or catecholamine release among Blacks.
Another behavioral factor associated with high blood pressure among Blacks
is the “John Henryism” behavioral pattern of hard work and determination
against overwhelming odds. James, Hartnett, and Kalsbeek (1983)
speculated that Blacks who exhibit this type of determination, but who also
have few resources to help them achieve their goals, may be at greatest risk
for developing hypertension (James, LaCroix, Kleinbaum, & Strogatz, 1984).
Furthermore, it has been found that low SES Blacks who are high in John
Henryism have a higher percentage of hypertension than persons who are
low in John Henryism or have a high SES (James, Strogatz, Wing, & Ramsey,
1987). Interestingly, no interaction of John Henryism with education or blood
pressure has been found for Whites, suggesting, as James and colleagues
(1983) noted, that this coping style may be particularly relevant to Black
populations.
The behavior of individuals high in John Henryism may actually increase
their exposure to stressful social and environmental circumstances. That is,
these individuals may continually strive to gain control over their
environment in spite of numerous barriers, thereby potentially exposing
themselves more frequently to frustrating and stressful situations. Whether
this exposure to behaviorally mediated chronic stress results in enhanced
SNS and altered sodium regulation remains to be empirically determined. It

has been reported, however, that active behavioral coping with acute
laboratory stressors enhances sodium retention (Light et al., 1983). It is this
active coping with real-life stressors that is the sine qua non of the John
Henryism pattern.
Several studies support the notion of active coping as a moderating variable
in laboratory reactivity and ambulatory monitoring situational effects. Saab
et al. (1997) found that during a speech stressor (active coping), Black men
responded with lower blood pressure, cardiac output, and heart rate changes
than did White men, White women, or Black women. They also reported
more inhibitory-passive coping, hostility, pessimism, and less social support
than other groups. Light et al. (1995) found that high effort coping in
addition to high job status predicted diastolic blood pressure at work and in
the laboratory for both Black and Whites. Job strain coupled with lower
status is also implicated in reactivity (K. A. Lawler & Schmied, 1992).
Chronic social stressors may also have other psychological and emotional
effects that could potentially influence sodium retention and neuroendocrine
release. For example, low income Blacks have been found to report more


psychological distress than low or high income Whites and high income
Blacks, perhaps due to the combined burden of poverty and racism (Kessler
& Neighbors, 1986). Additionally, the stressful residential environments to
which many Blacks are exposed (e.g., crowding and crime) are related to
stress symptoms, such as anxiety, depression, somatic complaints, lower
levels of perceived control, and enhanced sympathetic nervous system
activity (Baum et al., 1983; Davidson et al., 1987; Fleming et al., 1987;
Schaeffer & Baum, 1984). It has been suggested that urban Black youths
have decreased quality and quantity of social support. In fact, African
Americans residing in high poverty areas have a higher percentage of
people who report being unmarried, having no current partner, and having

no best friend compared with those living in nonpoverty areas. These
findings on the relative lack of potentially supportive social relationships
have also been observed in Whites (Belle, 1982). Social support has been
found to have both direct and indirect stress buffering effects on resting
blood pressure (Strogatz et al., 1997) and on cardiovascular reactivity
(Gerin, Milner, Chawla, & Pickering, 1995; Kamarck, Manuck, & Jennings,
1990; McNeilly et al., 1995).
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Biological and Genetic Factors
Although genetic variables have been identified as important in determining
sodium excretion in both Blacks and Whites (Luft, Miller, Cohen, Fineberg, &
Weinberger, 1988; Grim et al., 1984), epidemiologic evidence suggests that
the association of parental history and risk for hypertension may not be as
strong among Blacks relative to Whites (R. Stamler, J. Stamler, Riedlinger,
Algera, & Roberts, 1979). In fact, no published studies have reported the
expected relation between parental history of hypertension and
cardiovascular reactivity among Black adults (Anderson et al., 1986;
Anderson, Lane, Taguchi, & Williams, 1989; Anderson, Lane, Taguchi,
Williams, & Houseworth, 1989; Rowlands et al., 1982), although this relation
has been found fairly consistently among Whites (Fredrikson & Matthews,
1990). A possible explanation for these somewhat puzzling findings may be
the substantial influence of psychosocial factors in the development of
hypertension among Blacks. That is, psychosocial factors, such as chronic
stress, may overshadow the influence of parental history such that risk for
hypertension and hyperactivity are augmented even in persons with a
negative parental history. This could result in a diminished ability to detect
differences between parental history groups among Blacks.
Second, although sodium retention has a clear genetic component (Grim et
al., 1984), it may also be stimulated by psychosocial stress. To the degree

that Blacks, particularly low income Blacks, experience more psychological
stress than do Whites or upper income Blacks (Kessler & Neighbors, 1986),
they may consequently be more susceptible to inhibited sodium excretion.
Finally, the genetic distinction between Black and White Americans is, at
best, ambiguous. It has been noted that the gene pool of American Blacks is
comprised of a heterogeneous mixture of genes from genetically diverse
populations in Africa (Hiernaux, 1975; Mourant, 1983) and the U.S.
Caucasian population (Glass & Li, 1953; Pollitzer, 1958). In fact, Reed (1969)
estimated that up to 505 of the genes of Black Americans are derived from
Caucasian ancestors, whereas Lewontin and associates (Lewontin, 1973;
Lewontin, Rose, & Kamin, 1984) reported that genetic differences between
individuals within a race have a substantially greater impact on the total


species genetic variation than genetic differences between races. Therefore,
although genetic factors no doubt play a role in reactivity among Blacks,
their influence on between- race differences is likely to be considerably less.

Coping Resources
Thus far, the chapter has been discussing the various physiologic, social,
and behavioral factors that may contribute to the augmented sodium
retention, greater vascular reactivity, and higher hypertension prevalence
among Blacks as compared to Whites. It is important to note, however, that
there may be factors inherent in the culture and traditions of Black
Americans that may counteract the sympathetic and hypertensinogenic
effects of chronic stress. A number of researchers have advocated the view
that minorities share many characteristics (contextual, social, and
behavioral) associated with unique intra- and interethnic stress coping
mechanisms (Armstead, 1991; Dressler, 1993; Smyth & Yarandi, 1996;
Williams, 1996).

According to the contextual model, certain cultural traditions such as strong
kinship ties, unique forms of emotional expressiveness, social support, and
spirituality could decrease the effects of stress and consequently the effects
of stress on SNS activity, sodium retention, and blood pressure level. It has
been found, for instance, that resting blood pressure levels among Whites
who attend church regularly are lower than among those with less frequent
attendance (Graham et al., 1978). It would be of interest to determine
whether Blacks exposed to chronic life stressors (e.g., low income Blacks)
but who also have a high cultural “buffer” (e.g., strong religious orientation,
social support, or an extended family network) exhibit lower tonic SNS
activity, lower sodium retention, and lower cardiovascular reactivity than
those individuals less connected with cultural resources.
Because of the paucity of coping, stress, vulnerability, and resiliency
measures, the complexity of behavior in this population is often
misrepresented and misunderstood (Stevenson, 1997). It is important that
researchers perform ethnographic studies of culture, stress, and coping in
minority populations before making generalizations about psychosocial
mediators of cardiovascular reactivity. Furthermore, studies of behavioral
risk factors, adaptive behaviors, and maladaptive behaviors are warranted
from a culturally sensitive perspective (Bagley, Angel, Dilworth-Anderson,
Liu, & Schinke, 1995; Myers, Kagawa-Singer, Kumanyika, Lex, & Markides,
1995). It is imperative to understand how culture and ethnicity may interact
with the laboratory environment, the perceptions of laboratory stressors,
and the psychological and physiological coping responses to stressors.

TESTING THE CONTEXTUAL MODEL
Directions for Research
The contextual model presented here was designed to provide a stimulus for
examining both the basis for racial differences in vascular reactivity as well
as for exploring within-race variability in vascular responses among Blacks.

Toward these ends, the model suggests a number of testable hypotheses
and research questions. Various components of the model could be tested
using either field or laboratory methodologies. For example, the model
would predict that Blacks who are exposed to higher levels of chronic stress
should have higher resting stress hormone levels (e.g., catecholamines,


ACTH) and exaggerated responses to novel stimuli, suggesting increased
SNS activity compared to Blacks experiencing lower levels of chronic stress.
Second, chronic stress should also be positively associated with increased
sodium retention (i.e., slower sodium excretion rates) and greater vascular
reactivity in Blacks. Third, the combination of chronic stress exposure and
behavioral and psychological factors, such as anger suppression and John
Henryism, should be positively associated with both increased SNS activity
and greater sodium retention. Dietary sodium loading (or saline infusions)
should potentiate
-436vascular reactivity in Blacks experiencing chronic stress. Furthermore,
macrosocial phenomenon, such as lower SES, residence in socially unstable
communities, and chronic exposure to racial stress should be positively
associated with increased SNS activity and greater sodium retention. Finally,
the contextual model would predict that Blacks with more coping resources
(e.g., high social support, strong religious orientation, and racial identity) will
show lower SNS activity and decreased sodium retention relative to those
with fewer coping resources.

CONCLUSIONS

In summary, according to the proposed model, race is viewed as a
sociocultural designation that denotes differential exposure to chronic social
stressors. It is proposed that Black Americans are exposed to significantly

more chronic social stressors than White Americans. Many of these chronic
social stressors have been associated with hypertension prevalence in
epidemiological studies. Furthermore, chronic stress has been shown to
augment cardiovascular reactivity to acute stress in both animals and
humans and to increase sodium retention in SHRs. Acute stress has also
been demonstrated to increase sodium retention in humans. The essential
element of this model is that chronic social stressors that are
overrepresented within the Black American population due to historical
factors are related to an increase in sodium retention and enhanced
reactivity. This altered sodium metabolism and reactivity may be further
augmented by biological, behavioral, and psychological risk factors for
hypertension and modulated by stress coping resources. It is hoped that this
model will serve as a stimulus for further research on the biopsychosocial
aspects of autonomic reactivity and hypertension in minorities. Disparity in
health status will remain a problem in this country until researchers begin to
look at ethnic- specific pathways using this type of contextual modeling
approach. This is a challenge directed at researchers to test the applicability
of this model to other minority populations.