The Effects of Ethnic Discrimination and Socioeconomic Status on Endothelin-1 Among Blacks and Whites

Blacks in the United States have disproportionately higher rates of cardiovascular disease (CVD) than whites, including hypertension rates that are among the highest in the world. However, lower prevalence of hypertension is found among people of African descent in the Caribbean and West Africa.1 Thus, nongenetic influences likely contribute to black–white differences in CVD. Although blacks show higher levels of certain cardiovascular risk factors (e.g., obesity), their rates of other risk factors (e.g., hypercholesterolemia) are often similar or lower than whites.2 Ethnic differences in exposure to chronically stressful conditions, including lower socioeconomic status (SES), have been proposed as underlying contributors to disparities in cardiovascular health.3 Obesity and health behaviors partially explain the links established between lower SES and CVD,4 but stress-related physiological activation may also be a contributing factor.5,6 Blacks often report greater stressors than whites, even when both groups have similar SES. Prominently embedded within the larger context of SES are ethnic differences in certain stressors, such as discrimination.3 Perceived discrimination could increase cardiovascular risk by adding to the overall burden of chronic stress.7–10 Although higher SES often confers health advantages, its influence on the physical impact of discrimination-related stress is unclear. Perceived discrimination has been associated with adverse levels of several cardiovascular health indicators,11–14 particularly increased blood pressure (BP) reactivity.15,16 Assessments of BP partly reflect underlying systemic vascular resistance, which is elevated in hypertension and is largely influenced by vasoconstriction. However, few investigations have examined the effects of chronic stress on the biochemical regulation of vasoconstriction. Endothelin-1 (ET-1) is a potent vasoconstrictor that elicits long-lasting constriction of smooth muscle cells and induces proliferation of smooth vascular cells and cardiac myocytes.17,18 Plasma ET-1 largely reflects spillover from the vascular wall into the blood.18 Elevated ET-1 may contribute to vascular remodeling, renal dysfunction, atherosclerotic plaques, left ventricular hypertrophy, and other changes related to hypertension and heart failure.17,18 Higher ET-1 is linked to coronary heart disease19 and independently predicts mortality in patients with congestive heart failure and myocardial infarction.20 ET-1 is posited to modulate stress responses due to its distribution throughout the central nervous system, including the hypothalamus and the amygdala, which are thought to play an integrative role in physiological responses to stressful stimuli.21 However, the relationship between ET-1 in the central nervous system and circulating plasma ET-1 is uncertain. Blacks have shown higher resting ET-1 than whites,22–25 but not consistently.26,27 Given that ET-1 has a variety of possible influences,28 the mixed findings regarding ethnic differences may be partly due to confounding by uncontrolled or unknown variables. Despite the potential role of this vasoconstrictor in cardiopathogenesis, possibly via stress-induced increases,24,25,29 literature addressing its relationship to psychosocial characteristics is limited.26,30 No studies were found that examined ET-1 for ethnic differences in the effects of discrimination. However, research revealed an association between lower SES and higher ET-1, but no ethnic group comparisons were conducted.26 It is unknown whether SES shows similar influence across ethnic groups or whether discrimination makes a unique contribution to ET-1 beyond SES. Thus, the current study examined how resting plasma levels of ET-1 are related to SES and to ethnic discrimination among blacks and whites.