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.