ENDOTHELIUM AND CA-2+ IN THE PROSTAGLANDIN-F2-ALPHA POTENTIATION OF VASOCONSTRICTOR RESPONSES

Prostaglandin F2α (PGFP2α), at a concentration that did not induce vascular contraction (10-9 and 10-10 M), potentiated the dose-response curves to norepinephrine (NE) in rat mesenteric ring segments only when the endothelium was present. Moreover, PGF2α, in both unrubbed mesenteric artery and mesenteric vascular bed, was able to increase the contraction to NE as well as the ratio of the amplitude of two NE-induced contractions under previously standardized conditions, in the absence of extracellular calcium. In addition, without extracellular Ca2+, PGF2α increased in both tissues the refilling of Ca2+ induced by 80 mM KCl plus 1.5 mM Ca2+. The mechanism of this potentiation is unknown, but it may be related to cellular events including the intracellular Ca2+ mobilization. This study suggests that the endothelium plays a necessary role in PGF2α potentiation of vasoconstrictor response, possibly through the release of an endothelial vasoconstrictor factor which probably increases the Ca2+ bioavailability for the contraction. © 1990.