The renal response to converting enzyme inhibition and the treatment of sodium-sensitive hypertension.

Multiple lines of evidence suggest that intrarenal angiotensin AII formation participates in the control of renal perfusion and function. Inappropriate activation of this intrarenal system may participate in the pathogenesis of hypertension in about 45 percent of patients with essential hypertension, a group that we call "non-modulators" (NM). In NM the renal vascular response to AII is blunted when the subjects are on a high-salt diet, but appropriate when they are on a low-salt diet. Converting enzyme inhibition in NM induces a larger increase in renal blood flow, than occurs in normal subjects or other patients with essential hypertension, most evident when they are on a high-salt diet. The renal vasodilatation is not due to prostaglandin or bradykinin accumulation in the kidney, since the increase in renal blood flow induced by converting enzyme inhibition is associated with an enhanced renal vascular response to AII. When NM are shifted from a low to a high sodium intake, they show more positive sodium balance, gain more weight and increase their blood pressure more--the characteristics of sodium sensitive hypertension. Converting enzyme inhibition corrects their inability to handle a sodium load as it improves renal blood flow, and induces a depressor response that does not correlate with plasma renin activity. Many of these characteristics are shown in a normotensive offspring of essential hypertensives: since sodium handling is genetically determined, this abnormality may represent the inherited renal abnormality. An abnormality in the control of the renal circulation by AII, reversed by converting enzyme inhibition, may represent a fundamental abnormality in the pathogenesis.