Dysregulation of aldosterone secretion and its relationship to the pathogenesis of essential hypertension

Abstract

The level of sodium intake has a reciprocal influence on the vascular and adrenal responses to angiotensin II, with sodium restriction enhancing the adrenal responses and reducing vascular, and particularly renal vascular, responses. In two subgroups of the essential hypertensive population, this relationship is abnormal. Both subgroups have sodium-sensitive hypertension. One is a subset of the low renin essential hypertensive subgroup and its abnormality is an enhanced aldosterone response to angiotensin II with sodium loading, ie, a failure to down-regulate the aldosterone response. The other subgroup, termed nonmodulators, is a subset of the normal-high renin essential hypertensive subgroup. In these patients, sodium intake modifies either adrenal or vascular responses, including renal vascular responses, to angiotensin II--resulting in a reduced aldosterone response to angiotensin II with sodium restriction. Of clinical importance, the nonmodulator's abnormality is corrected by the administration of converting enzyme inhibitors--this class of drugs therefore being a specific form of therapy in these patients.