Low-Renin Essential Hypertension: Diminution of Aldosterone Suppression?
Renin profiling of hypertensive patients has led to the identification of a subgroup of patients with low-basal plasma renin activity (PRA) that does not increase in response to various maneuvers known to stimulate PRA in normal individuals. A small percentage of these individuals subsequently is found to have primary aldosteronism or glucocorticoid-suppressible hypertension, but the majority have normal plasma aldosterone concentrations. Despite differences in the methods of ascertainment of PRA and the stimuli applied to induce renin release, as well as difficulties in obtaining controls that are appropriately matched for age, sex, and race (1, 2), most investigators have identified suppressed PRA in 17%—46% of patients with essential hypertension (3). Yet, despite its prevalence, the pathophysiology of low- renin essential hypertension (LREH) remains obscure. In this paper, we will attempt to summarize what is known about LREH, particularly with respect to adrenal function, and propose a hypothesis of the pathophysiology involved.
KeywordsDopamine Serotonin Norepinephrine Catecholamine Theophylline
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