Evidence against the involvement of prostaglandins in the vasoconstrictor action of @entity460 ion in XXXX mesenteric blood vessels.

@entity2871 @entity3351 @entity1421 @entity141 @entity2872 @entity3009 @entity3302 @entity460 @entity35 @entity3352 @entity20292 @entity1063
1. @entity1421 ( @entity1421 ) has been claimed to be essential to the vasoconstrictor action of @entity1063 in @entity35 mesenteric blood vessels. Since @entity1063 acts by releasing intracellular @entity460 , experiments have been performed using the perfused @entity35 superior mesenteric artery preparation to determine whether @entity3009 synthesis is necessary for the direct vasoconstrictor action of @entity460 . 2. The cyclo-oxygenase inhibitors, @entity3352 and @entity3351 ( @entity20292 ), inhibited responses to @entity1063 and @entity460 but both were less effective in inhibiting the response to @entity460 than to @entity1063 . 3. @entity1421 (6 ng-20 micrograms/ml) failed to overcome the inhibitory effect of @entity3352 (62 micrograms/ml) and ETA (10 micrograms/ml) on the response to the EC50 of @entity141 (100 micrograms/ml). The EC50 of @entity141 did not significantly increase @entity1421 -like release by the blood vessels from the resulting value of 19 +/- 8 pg of @entity1421 equivalents/min. 4. PGA1 (6 micrograms/ml) and the @entity2871 A2 agonist, @entity2872 (200 ng/ml), both caused full restoration of @entity3352 -depressed responses to @entity460 , but did not restore responses depressed by ETA. @entity2872 (200 ng/ml) also reversed the inhibitory effect of @entity3302 (4 micrograms/ml) and caused a 1.6 fold potentiation of @entity141 responses. 5. The results do not support the hypothesis that @entity3009 synthesis is essential to the vasoconstrictor action of @entity141 in @entity35 mesenteric blood vessels.
