Why the study?
Does obesity alter plasma renin activity and aldosterone levels in patients with essential hypertension?
Does obesity alter plasma renin activity and aldosterone levels in patients with essential hypertension?
Obesity in essential hypertension is associated with an inappropriately high aldosterone-to-renin ratio, which may contribute to sodium and water retention and promote hypertension.
Obesity-associated PRA suppression with unchanged aldosterone may promote sodium retention in hypertension; leaves open causal mechanisms and targeted interventions.
The possible role of obesity in the development of hypertension was investigated in two study groups. In a population study of 961 subjects, 739 were found to be normotensive and 222 hypertensive. The prevalence of hypertension was 18.7 percent in the nonobese, and 33.2 percent in the obese subjects. Systolic and diastolic blood pressures increased progressively with the increase of relative body weight in both normotensive and hypertensive subjects. In addition, an endocrinologic study was made of 97 patients with essential hypertension; in 82, plasma renin activity (PRA) was inversely correlated with the increase of relative body weight but not with urinary Na excretion. Despite this decrease of PRA, the level of serum aldosterone was not influenced by relative body weight. Thus, the aldosterone/PRA ratio ratio increased progressively with the increase of relative body weight. Thiazide therapy normalized this inappropriately high ratio, and reduced body weight and blood pressure. Restriction of dietary calories and salt intake had a similar effect. With a high-salt intake in an obese subject, the aldosterone/PRA ratio is unduly increased. Apparently aldosterone contributes to the additional retention of sodium and water and thereby promotes hypertension in the presence of an expanded fluid volume.
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Hiramatsu et al. (1981) studied this question.
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