Effects of captopril on blood pressure and renin-angiotensin-aldosterone system in hypertensive subjects after inhibition of renal vasodilative system.
The aim of this study is to contribute to the understanding of the probable role of the renin-angiotensin-aldosterone, the kallikrein-kinins and the prostaglandins systems on the various types of essential hypertension and also their contribution to the action of captopril. Nineteen patients, 7 with high and 12 with normal or low levels of plasma renin activity (PRA), have been studied. Captopril (100 mg) was administered in acute dosage, blood pressure was checked for two hours and PRA and plasma aldosterone were assayed. The same trial was repeated after inhibition of prostaglandin-synthetase with indomethacin and kallikrein with trasylol, alternatively, and then with indomethacin and trasylol, contemporaneously. Our results showed that the renal vasodilative system was probably also involved in the mechanism of action of captopril, but that this drug reduced blood pressure mainly through a block of angiotensin II production in both groups of patients. Thus the finding of a normal or low PRA does not justify the conclusion that angiotensin II is not one of the mechanisms responsible for an elevated arterial pressure.
D000809:Angiotensins / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects*; D002216:Captopril / Q000494:pharmacology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D011392:Proline / Q000031:analogs & derivatives*; D012079:Renal Circulation / Q000187:drug effects*; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects*
D000809:Angiotensins; D011392:Proline; D002216:Captopril; D012083:Renin