Converting enzyme inhibition: implications for renal perfusion and function.

Abstract

1. Substantial but circumstantial evidence has suggested an important role for angiotensin in the control of renal perfusion and function. A local, intrarenal action may have been angiotensin's first role in phylogeny, additional actions on the adrenal and the systemic vasculature having arisen later. 2. Converting enzyme inhibitors, both teprotide and captopril, induce a potentiated renal vascular response in patients with essential hypertension, associated with a consistent increase in sodium excretion and occasionally an increase in glomerular filtration rate. In patients with advanced congestive heart failure resistant to other vasodilators, a similar triad occurs. 3. It is not yet clear in which settings the renal response to converting enzyme inhibition reflects a reduction in angiotensin II formation thus implicating the reninangiotensin system in the pathogenesis; or an additional action, such as a potentiation of the local actions of bradykinin or enhanced prostaglandin formation. 4. Under some circumstances, especially where a qualitatively and quantitatively similar response occurs to angiotensin antagonists and converting enzyme inhibitors or where an angiotensin antagonist prevents an additional response to a converting enzyme inhibitor, the specific action of the converting enzyme inhibitor of angiotensin II formation is clearly responsible. Unfortunately, for most responses in animal models and all responses in patients such rigorous evidence is not yet available.