Effects of Prostaglandin F^ on Vasoconstrictor Responses in the Mesenteric Vascular Bed

Prostaglandin F^ (PGFjJ In a concentration that did not induce vascular contraction (10~ M) potentiated the dose-response curves to norepinephrine and 5-hydroxytryptamine and the contractile response induced by potassium (60 or 100 mM) in isolated mesenteric vascular bed of the rat. After prostaglandin inhibitor treatment with indomethacin (10~ M), the dose-response curve to norepinephrine was reduced, and the dose (10" M) of PGF ,̂, which was ineffective hi control tissues, facilitated the norepinephrine contractile response. In contrast, indomethacin did not change either the contractile response induced by potassium or the PGF^ potentiation of this response. Calcium antagonists diltiazem or flunarizine reduced the potassium-induced contractile response. After diltiazem treatment, 10" M of PGF^ was also effective in facilitating this response. The PGF^ postjunctionaJ effect was conserved after phosphoinositide hydrolysis inhibition. These results suggest that PGF^ potent iat ion of the contractile response may be independent of PGF^ contraction. Low doses of endogenous prostaglandins could be able to facilitate the norepinephrine contractile response in this tissue. This process may be independent of calcium influx and phosphoinositide hydrolysis. (Hypertension 11 [Suppl I]: I-108-I-111, 1988)