SAN ANTONIO — Increased levels of adrenal steroids appear to contribute to metabolic syndrome in African Americans, Dr. Theodore A. Kotchen said at a meeting of the American Heart Association Council for High Blood Pressure Research.
“We speculate that the finding of a relatively high plasma aldosterone and low plasma renin activity in hypertensive African Americans may represent a forme fruste or mild variant of the spectrum of disorders that we refer to as primary aldosteronism,” said Dr. Kotchen, professor of medicine at the Medical College of Wisconsin, Milwaukee.
The prevalence of hypertension in African Americans is among the greatest in the world. Their hypertension-related cardiovascular event rates are also high.
To examine the relationship between adrenal steroids—specifically, aldosterone and cortisol—and metabolic syndrome risk factors in African Americans, Dr. Kotchen and his coinvestigators studied 182 hypertensive and 215 normotensive African Americans aged 18–55 years in an inpatient clinical research unit. Roughly half were women. All subjects had temporarily discontinued antihypertensive and lipid-lowering medications weeks beforehand.
The mean plasma aldosterone value of 8.4 ng/dL in hypertensive subjects was significantly higher than the 6.3 ng/dL in normotensives. Both late-night and early-morning salivary cortisol levels were significantly higher in hypertensive individuals as well.
In contrast, plasma renin activity was inversely related to blood pressure, indicating that the increase in aldosterone in hypertensive African Americans isn't renin mediated.
Overall, 17% of study participants met criteria for metabolic syndrome. Plasma aldosterone levels were significantly higher in those with metabolic syndrome than in those without it.
Moreover, both aldosterone and blood pressure were significantly correlated with each of the individual elements of metabolic syndrome: waist circumference, cholesterol, triglycerides, body mass index, low HDL cholesterol, plasma insulin, and insulin resistance. In other words, hypertensive subjects as well as those with higher plasma aldosterone had greater waist circumference, more insulin resistance, and more unfavorable lipid profiles.
Based upon these observations, Dr. Kotchen offered the following speculation: Environmental and perhaps genetic factors contribute to the development of central obesity, which triggers increased activity of β-hydroxysteroid dehydrogenase in visceral adipose tissue. This enzyme converts metabolically inactive cortisone into active cortisol, which promotes adipogenesis and adipose tissue hypertrophy in target tissues, creating a vicious cycle that leads to further increases in cortisol.
Elevated cortisol levels result in hyperinsulinemia and insulin resistance. And there is evidence from animal and in vitro studies to suggest that elevated insulin stimulates aldosterone production through a renin-independent mechanism.
Alternatively, it's possible that fatty acids present in adipose tissue stimulate aldosterone production independent of insulin's actions. In any case, the increased aldosterone promotes sodium retention, resulting in both elevated blood pressure and a reduction in renin secretion, Dr. Kotchen explained.