Abstract
The aim of the present investigation was to elucidate the pharmacological mechanism by which U44069, a stable PGH2 analogue, contracts the rat aorta. The results obtained demonstrate that while the contractile effect of potassium chloride is obliterated by removal of extracellular calcium, a substantial proportion of the contractile effect of U44069 persists under these conditions. The persistent effect of U44069 under calcium-free conditions was not diminished by nifedipine (a slow calcium channel blocker) but was blocked by 2-n-butyl-3-dimethylamino-5,6-methylenedioxyindene (an intracellular calcium antagonist). These results provide experimental evidence for the proposal that U44069 contracts the aorta in the absence of extracellular calcium by mobilizing intracellular calcium.
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