Angiotensin converting enzyme inhibitors (captopril, CGS14831 and CGS14824A) antagonisein vitro smooth muscle prostanoid synthesis: evidence for calcium channel blockade

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Abstract
The present study investigated the effect of the angiotensin-converting enzyme (ACE) inhibitors, captopril, CGS14824A and CGS14831 onin vitro rat aortic and urinary bladder prostacyclin (PGI2; measured as 6-oxo-PGF1α by radioimmunoassay) synthesis. PGI2 synthesis was stimulated with adrenaline (aorta), carbachol (bladder), calcium ionophore A23187, arachidonate and trauma. The ACE inhibitors antagonised adrenaline-, carbachol- and A23187-stimulated PGI2 synthesis in the aorta and bladder (CGS14824A>captopril>CGS14831) but were without effect on trauma- or arachidonate-stimulated PGI2 synthesis. The patterns of inhibition of these ACE inhibitors, using the same stimulatory regimes, was very similar to those previously observed by us with known calcium channel blockers (nifedipine, verapamil). These data suggest that: (i) ACE inhibitors possess calcium channel blocking properties, which may be of relevance to the antihypertensive action of these drugs; and (ii) ACE inhibitors did not stimulate vascular PGI2 synthesis as has been previously suggested.