Rapoport R M
Department of Pharmacology and Cell Biophysics, University of Cincinnati, College of Medicine, OH 45267-0575.
Eur J Pharmacol. 1993 Oct 19;243(2):207-10. doi: 10.1016/0014-2999(93)90382-r.
This study investigates the role of primary prostaglandin receptor activation in the modulation of agonist-induced vascular smooth muscle contraction. Prostaglandin F2 alpha induced a concentration-dependent contraction of the rat aorta that was nearly abolished by the thromboxane A2 receptor antagonist, SQ29548. Prostaglandin F2 alpha 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 F2 alpha 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 Ca2+ channels.
