Abstract

This study investigates the role of primary prostaglandin receptor activation in the modulation of agonist-induced vascular smooth muscle contraction. Prostaglandin F 2α induced a concentration-dependent contraction of the rat aorta that was nearly abolished by the thromboxane A 2 receptor antagonist, SQ29548. Prostaglandin F 2α in the presence of SQ29548 induced leftward shifts of the norepinephrine and KCl concentration-response curves. Nifedipine abolished the leftward shift of the norepinephrine concentration-response curve observed in the presence of prostaglandin F 2α and SQ29548. These results suggest that a function of primary prostaglandin receptor activation may be to potentiate agonist-induced contraction. The potentiation is dependent upon the opening of dihydropyridine-sensitive Ca 2+ channels.

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