Converting enzyme inhibition and the kidney.
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 renin-angiotensin 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 clear 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.
D000804:Angiotensin II / Q000037:antagonists & inhibitors; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000502:physiology*; D007677:Kidney Function Tests; D011817:Rabbits; D012039:Regional Blood Flow; D012964:Sodium / Q000502:physiology; D013722:Teprotide / Q000494:pharmacology; D014666:Vasomotor System / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D012964:Sodium; D013722:Teprotide