Difference in prostaglandin modulation of arterial and venous smooth muscle responses to bradykinin and norepinephrine.

The role of endogenously synthesized prostaglandins as modulators of canine vascular smooth muscle responses to bradykinin (BK) and norepinephrine (NE) was evaluated in vitro with the use of helical strips of canine arteries and veins and measurement of prostaglandins with bioassay and thin layer chromatography. Inhibition of prostaglandin synthetase with indomethacin (INDO) resulted in a small, but significant, enhancement of the contractile responses of mesenteric and splenic arteries and portal veins to NE. Eicosatetraynoic acid (ETYA), another inhibitor of prostaglandin synthetase, did not affect the contractile responses of canine splenic and mesenteric arteries and portal veins to NE. ETYA (1 x 10(-5) M), inhibited prostaglandin biosynthesis. Addition of INDO to arterial smooth muscle strips, in which prostaglandin synthesis was inhibited with ETYA, also resulted in consistent enhancement of the responses to NE. INDO did not effect the contractile responses of canine mesenteric and splenic veins to NE. BK-induced relaxation of canine mesenteric, but not splenic, arteries was inhibited by INDO, INDO did not effect BK-induced contraction of splenic, mesenteric or portal veins. ETYA was without effect on the responses of either arteries or veins to BK. After inhibition of prostaglandin synthetase with ETYA, INDO was still an effective inhibitor of BK-induced relaxation of arterial smooth muscle. Tranylcypromine (1 x 10(-5) M) inhibited prostacyclin (PGI2) synthesis but did not affect the responses of the vascular smooth muscle to BK or NE. These findings are consistent with the conclusion that in canine vascular smooth muscle in vitro, endogenously synthesized prostaglandins do not modulate the contractile responses to NE or BK. The data also confirm the presence of a direct vascular smooth muscle action for INDO.