Therapy of Hypertension in African Americans

John M. Flack; Samar A. Nasser; Phillip D. Levy


Am J Cardiovasc Drugs. 2011;11(2):83-92. 

In This Article

1. Pathogenesis of Hypertension

There are no unique risk factors for hypertension between racial/ethnic groups. However, some pathophysiological mechanisms that are etiologically linked to the development of hypertension do tend to be disproportionately prevalent in selected racial/ethnic groups. The pathophysiological perturbations discussed in sections 1.1–1.4 represent tendencies that occur more commonly in African Americans than in Whites.

1.1 Obesity

Obesity contributes significantly to hypertension risk in all populations, particularly racial and ethnic minorities. Obesity is more prevalent in both African Americans and Hispanics, particularly in women, compared with Whites.[7] More importantly, nearly one in six African American women are considered extremely obese (body mass index [BMI] >40 kg/m2); this prevalence is almost 4-fold higher than that of either White or Hispanic women. There are also marked ethnic and agebased differences in the rate of weight accumulation with an earlier onset of obesity in African Americans versus Hispanics (for women) and Whites (for men).

Obesity-related physiological effects that contribute to the intermediate BP phenotype include enhanced sympathetic activity,[8] altered salt sensitivity (see also section 1.2),[9,10] and resistance to antihypertensive drug therapy.[11,12] Additionally, obesity appears to be a plausible mediator of chronic renal injury[10,13] and is a known contributor to sleep-disordered breathing.

1.2 Salt Sensitivity

Salt sensitivity is disproportionately manifest in African Americans, particularly among those with hypertension. Salt sensitivity can conceptually be defined as a rise in BP occurring during salt administration and/or a fall in BP occurring when salt is restricted. The excess prevalence of salt sensitivity among African Americans relates to the increased frequency of obesity in this population. It has been demonstrated in both Caucasians and African Americans that obesity is linked to salt sensitivity[14,15] and that weight loss ameliorates salt sensitivity, at least among overweight Caucasian adolescents.[14] Low dietary potassium intake in all likelihood substantively contributes to salt sensitivity as high levels of potassium intake can nearly ameliorate the pressor effect of salt in salt-sensitive African Americans.[16] Salt sensitivity has been linked to a lesser fall in nocturnal BP as well as to microalbuminuria and other pressure- related target-organ injury. Salt sensitivity has also been linked to higher antihypertensive medication requirements.

1.3 Renin-angiotensin System

There has been pervasive interpretation of the tendency toward lower circulating renin levels and a lesser average BP reduction in response to monotherapy with renin-angiotensin system (RAS) antagonist drugs (e.g.ACE inhibitors) compared with diuretics in African Americans as being indicative of a relative inactive RAS system. Low circulating renin levels, however, have been linked to augmented vascular production of angiotensin II,[17] and normotensive, healthy African Americans have been shown to have more, not less, activation of the RAS system than Whites.[18] Circulating aldosterone levels are also higher in African Americans than in Whites.

The exact role of the RAS system in African Americans has not been defined. However, given the pattern of excessive RAS system-dependent target-organ injury (e.g. left ventricular hypertrophy, chronic kidney disease/proteinuria) in African Americans, it is likely that the importance of the RAS system has been overly discounted in this population.

1.4 Vascular Function

Endothelium-dependent and endothelium-independent vascular responses are abnormal in African Americans com- pared with Whites.[19,20] There are potentially explanatory data suggesting that the bioavailablity of nitric oxide, the main determinant of endothelium-dependent vascular function, is lower in African Americans than in Whites even though African Americans have much higher endothelial-derived nitric oxide synthase (eNOS) activity.[21] It appears that the synthesis of oxygen radicals, mostly via uncoupled eNOS and lesser amounts via NADPH (nicotinamide adenosine dinucleotide phosphate) oxidase, raises levels of oxidative stress and accelerates nitric oxide destruction, which leads to reduced nitric oxide bioavailability/activity in African Americans.[21]


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