Aldosterone and Hypertension in African Americans

Hypertension is more prevalent, more difficult to treat, and more associated with morbidity among African Americans than among Caucasians. Hypertension in African Americans is usually salt sensitive and is associated with low plasma renin activity. This has led many to believe that the kidneys of these patients might have a lower ability to excrete a sodium load because of congenital or acquired alterations in renal sodium transport mechanisms. In this issue of the American Journal of Hypertension, Kidambi et al.1 highlight some interesting issues regarding the role of aldosterone in the pathogenesis and treatment of hypertension in African Americans. They observed that, when stratified by BMI, hypertensive subjects in each BMI group had higher aldosterone and lower PRA as compared to normotensive subjects. This suggests that aldosterone may play an important pathogenic role in hypertension in African Americans, and that aldosterone antagonists may be useful in the management of these patients. Several studies have shown that, despite their low-renin state, African Americans with hypertension have elevated aldosterone levels as compared to similar subjects of other races; however, there has been no finality regarding the role that aldosterone antagonists should play in the treatment of hypertension in African Americans. In contradiction of the earlier hypothesis that angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are less effective in African-American populations, data from the AASK trial has demonstrated that renin–angiotensin blockade may, in fact, be of significant benefit in the treatment and prevention of hypertension-mediated renal end-organ damage in African Americans.2 Given that ACE inhibitors and ARB reduce aldosterone levels, the relative contributions of aldosterone and angiotensin II inhibition cannot be ascertained from this study. As a natural extension of the renin–angiotensin system, an aldosterone blockading agent would make sense as the next antihypertensive agent of choice, given that African Americans show a propensity toward mild hyperaldosteronism. Saha et al., as well as other groups, have recently shown the benefit of adding epithelial sodium channel inhibitors such as spironolactone and amiloride to conventional regimens in treating resistant hypertension in African Americans.3 One issue that has not been adequately addressed by Kidambi et al. is the possible contribution of dietary potassium to hypertension in African Americans. Urinary potassium excretion was lower in the hypertensive group of obese and overweight participants than in the normotensive group. Moreover, stepwise linear regression analyses showed that sodium excretion was directly related to blood pressure and potassium excretion was inversely related to blood pressure in obese patients. This suggests that a lower dietary potassium intake may contribute to hypertension in obese African Americans.4 Another matter of debate is the issue of underdiagnosis of true hyperaldosteronism in patients with hypertension. Several studies have suggested that hyperaldosteronism may be a more significant contributor to hypertension than has been previously recognized, especially in African Americans.5 The question that should be asked, therefore, is whether the higher prevalence of hypertension in African Americans, especially resistant hypertension, could possibly be secondary to underdiagnosed primary hyperaldosteronism. All the subjects included in the study by Kidambi et al. carried a diagnosis of essential hypertension, but there is no mention of how this diagnosis was made, and whether primary hyperaldosteronism was excluded. The authors declared no conflict of interest.