Effect of trifluoperazine, a calmodulin antagonist, on prostaglandin output from the guinea-pig uterus

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Abstract
Trifluoperazine, a calmodulin antagonist, inhibited the [calcimycin] A23187-induced increase in outputs of prostaglandin (PG) F-2.alpha. and 6-oxo-PGF-1.alpha. from the day 7 and day 15 guinea-pig uterus superfused in vitro. The basal outputs of, and the arachidonic acid-induced increase in outputs of PGF-2.alpha., PGE-2 and 6-oxo-PGF-.alpha. from the guinea-pig uterus were not inhibited by trifluoperazine. Indomethacin inhibited A23187-stimulated, arachidonic acid-stimulated and the basal outputs of PG from the guinea-pig uterus, indicating that trifluoperazine was not inhibiting cyclo-oxygenase. Since the action A23187 is dependent upon extracellular Ca2+, calmodulin is evidently involved in Ca2+-induced increases in uterine PG output from the guinea-pig uterus. Trifluoperazine, but not indomethacin, inhibited A23187-induced contraction of the guinea-pig uterus, which is consistent with calmodulin being involved in smooth muscle contraction. Arachidonic acid treatment did not contract the guinea-pig uterus. PG are apparently not involved in the contraction induced by A23187. Trifluoperazine caused a small, sometimes significant (P < 0.05), increase in uterine PG output. Exogenous arachidonic acid failed to increase PGF-2.alpha. output from the day 15 uterus in contrast to the stimulant action of A23187. Exogenous arachidonic acid caused a fairly large increase in uterine PGE-2 output in contrast to the small effect with A23187.

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