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POTENTIATION OF DEPRESSOR RESPONSES TO ARACHIDONIC ACID BY ANGIOTENSIN CONVERTING ENZYME INHIBITORS IN THE RAT
Author(s) -
Hui SC. G.,
Dai S.,
Ogle C. W.
Publication year - 1984
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1984.tb00875.x
Subject(s) - arachidonic acid , long term potentiation , enzyme , chemistry , angiotensin converting enzyme , endocrinology , pharmacology , angiotensin ii , medicine , biochemistry , biology , blood pressure , receptor
SUMMARY 1. In chloralose anaesthetized rats, intravenous administration of captopril, SQ 20881, SA 446 or MK 421 (0.5 mg/kg) potentiated the depressor responses to arachidonic acid 3 mg/kg given intravenously. 2. Same doses of the above angiotensin converting enzyme inhibitors caused an approximately 100‐fold decrease in sensitivity to the pressor effects of angiotensin I, with a concomitant similar increase in sensitivity to the depressor effects of bradykinin. 3. Depressor responses to arachidonic acid, both before and after administering the converting enzyme inhibitors, were abolished by intravenous indomethacin (5 mg/kg). 4. These results suggest that increased synthesis of prostaglandins in the circulation may contribute to the hypotensive effect of the angiotensin converting enzyme inhibitors, a group of newly developed antihypertensive agents.