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MECHANISMS OF CAPTOPRIL‐INDUCED POTENTIATION OF THE DEPRESSOR RESPONSES TO ARACHIDONIC ACID IN RATS
Author(s) -
Hui SC. G.,
Dai S.,
Ogle C. W.
Publication year - 1986
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.1440-1681.1986.tb00325.x
Subject(s) - captopril , long term potentiation , arachidonic acid , endocrinology , chemistry , pharmacology , medicine , blood pressure , biochemistry , enzyme , receptor
SUMMARY 1. The mechanisms underlying potentiation by captopril of the depressor responses to arachidonic acid were studied in chloralose‐anaesthetized rats. 2. Captopril, in a dose (0.5 mg/kg, i.v.) which inhibited the pressor responses to angiotensin I (0.03‐1 μg/kg, i.v.), enhanced the depressor responses to bradykinin (3‐300 μg/kg, i.v.) and potentiated the hypotensive action of arachidonic acid (3 mg/kg, intravenously). This phenomenon was observed not only when captopril and arachidonic acid were administered intravenously, but also when these compounds were injected directly into the aortic arch. 3. The enhancement of arachidonic acid‐induced hypotension by captopril was not significantly affected by pretreatment with a low dose of aprotinin (3 mg/kg, i.v.), but was abolished by bilateral nephrectomy or by pretreatment with a higher dose of aprotinin (6 mg/kg, i.v.). 4. It is suggested that captopril augments the depressor responses to arachidonic acid by inhibiting angiotensin converting enzyme. This results in accumulation of bradykinin which in turn increases release of vasodilator prostaglandins, originating most probably, from the kidneys. The possibility that blockade of angiotensin II formation by captopril may leave the vasodilator action of prostaglandin unopposed cannot be excluded.