Overview of the role of angiotensin inhibitors in delineating the function of the renin-angiotensin system.
In conscious sodium-deficient dogs, beta-adrenergic blockade with propranolol and angiotensin II receptor blockade with an angiotensin II inhibitory analogue reduced arterial blood pressure and increased urinary sodium excretion significantly, but the hypotensive and natriuretic response was considerably greater during inhibition of angiotensin I converting enzyme with captopril. Angiotensin II infusion (3 ng/kg/min) into sodium-deficient dogs maintained on captopril administration restored arterial blood pressure, urinary sodium excretion, and plasma aldosterone concentration to levels that existed in untreated sodium-deficient dogs. This indicates that the hypotensive and natriuretic actions of captopril are due to the inhibition of angiotensin II formation and not to the accumulation of the vasodepressor peptide, bradykinin.
D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000031:analogs & derivatives*; D000809:Angiotensins / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D004285:Dogs; D011392:Proline / Q000031:analogs & derivatives*; D011433:Propranolol / Q000494:pharmacology*; D012083:Renin / Q000502:physiology*; D012504:Saralasin / Q000494:pharmacology*; D012964:Sodium / Q000172:deficiency / Q000378:metabolism*
D000809:Angiotensins; D000804:Angiotensin II; D000450:Aldosterone; D011392:Proline; D002216:Captopril; D012964:Sodium; D011433:Propranolol; D012083:Renin; D012504:Saralasin