Converting enzyme inhibition and the kidney.

Abstract

SUMMARY We review information on the renal response to converting enzyme inhibition, and attempt to evaluate the evidence that a reduction in angiotensin II formation is responsible for the renal response. There is little response to converting enzyme inhibitors in animals or man when the renln-angk>tensin system is suppressed by a literal sodium intake. With restriction of sodium intake, an increase in renal blood flow occurs; because a quantitatively similar response occurs to the angiotensin II analogs it is likely that the response reflects reversal of the local action of angiotensin II. In other settings it is not yet dear whether the renal response to converting enzyme inhibitor reflects only a reduction in angiotensin II formation or an additional action such as potentiation of the local actions of bradykinin or enhanced prostaglandin formation. Because these agents induce a potentiated increase in renal blood flow in the patient with essential hypertension, and with it an increase in glomerular filtration rate and sodium excretion in some patients, despite a fall in arterial pressure these questions have considerable importance. suggested that angiotensin, in addition to its systemic effect on blood pressure (BP) and on sodium homeostasis through control of aldosterone secretion, may have a direct action on the renal blood supply. 18 The important conceptual role played by ablation in defining the action of a hormone in an effector system was pointed out by Haber. 4 In the special case of the interaction of the renin-angiotensin system and the kidney, the kidney is both the source of the hormone and the responding organ. The ablation experiment, therefore, has clearly been impossible. For that reason, the development of several classes of agent that have made it possible to interrupt the renin-angiotensin system pharmacologically has made a major contribution to the evolution of our ideas.Before we convert pharmacologic responses to a physiologic interpretation, it is important that we assess the specificity of the available agents. The two

The effects of combined angiotensin converting enzyme inhibition and β‐adrenoceptor blockade on plasma renin activity in anaesthetized dogs

“…These observations have established the importance of the renal sympathetic innervation as one of the primary controls of renin release, hence it is possible that the renal sympathetic innervation also contributes to the renin response to ACE-inhibition. The cardiovascular effects that accompany ACE-inhibition, such as local and systemic blood pressure and flow changes (McCaa et al, 1978;Meggs & Hollenberg, 1980;Johnston, 1984;Cambridge et al, 1988), are essentially 'pro-renin release' and may therefore provide the relevant stimuli to initiate an increased sympathetic drive to the kidney. There is some circumstantial evidence from studies in anaesthetized animals which lend further support to this idea.…”

Reduction of plasma and urinary vasopressin during treatment of severe hypertension by captopril

“…Contrary to other antihypertensive drugs like reserpine, guanethidine, methyl dopa, clonidine or vasodilators [ 121, converting enzyme inhibitors produce a fall in blood pressure without any sodium retention or increase in plasma volume [13][14][15][16].…”

Preservation of Renal Function in Chronic Renal Failure.

“…In man captopril has been reported to increase RBF in patients with essential hypertension (De Bruyn et al 1979;Reubi 1984) and normal subjects (Hollenberg et al 1981). Meggs and Hollenberg (1980) in a review of CET and the kidney concluded that there is little response to CET in animals or man when the renin-angiotensin system is suppressed by high sodium intake, but with sodium restriction RBF is increased by CEI.…”