Evidence for prejunctional inhibition of norepinephrine release by captopril in spontaneously hypertensive rats.
Pretreatment of spontaneously hypertensive rats (SHR) with the converting enzyme inhibitor captopril (10 or 100 mg/kg p.o.) had no effect on pressor responses to angiotensin II or norepinephrine whereas the response to angiotensin I was markedly inhibited. In contrast, pressor responses to sympathetic stimulation in pithed SHR were inhibited by captopril whereas the positive chronotropic responses to stimulation were unaltered. These results suggest that captopril causes a prejunctional inhibition of norepinephrine release to sympathetic nerve stimulation which is selective for the vasculature. This is probably due to inhibition of angiotensin II formation in the vasculature.
D000804:Angiotensin II / Q000096:biosynthesis; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000503:physiopathology*; D009638:Norepinephrine / Q000378:metabolism*; D011392:Proline / Q000031:analogs & derivatives*; D051381:Rats; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology
D000804:Angiotensin II; D011392:Proline; D002216:Captopril; D009638:Norepinephrine