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 hypert
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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Communicable and infectious diseases, the major causes of premature death in the United States prior to 1930, have been replaced by chronic illnesses such as heart disease and cancer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
Trang 20.8%), 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 )
-427-FIG 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 Hispanic Whites and higher than
Trang 3non-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
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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
Trang 4who 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
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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)
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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
Trang 5may 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
Trang 6pathogenesis 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
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stressors, 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
Trang 7lead 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
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and 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
Trang 8Armstead (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,
Trang 91989), 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 2-year 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
-433-to 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
Trang 10scenario 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