Potentiation of the algogenic action of bradykinin by an inhibitor of angiotensin I converting enzyme, captopril (SQ 14,225).

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Experiments were conducted on II loosely restrained, conscious dogs which responded with vocalization in a dose-dependent manner to bradykinin (0.6-10 nmol) or acetylcholine (0.1-10 μmol) injected into the femoral or the mesenteric artery through a chronically indwelling arterial catheter. Vocalization was taken as being to reflect the algogenic action of these substances. Administration of captopril (1 mg/kg, i.v.) potentiated the algogenic action of bradykinin but not that of acetylcholine injected into either artery. The magnitude of potentiation of the algogenic action was about 3-fold for bradykinin injected into the femoral artery and about 10-fold for that injected into the mesenteric artery. The potentiation can be interpreted in terms of inhibition of kininase II by captopril. The difference in potentiation by captopril of the algogenic action of bradykinin injected into the two arteries may reflect the difference in kininase II activity in the two arterial beds. Possible involvement of E-series prostaglandins in the potentiation was also discussed.
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