Dopamine-induced potentiation of the contractile response to arachidonic acid in guinea-pig aorta.
In guinea-pig aorta, the potentiating effect of dopamine on the response to arachidonic acid was examined. The potentiation by dopamine was completely abolished by nordihydroguaiaretic acid, but not by indomethacin, aspirin, corticosterone, haloperidol, SK & F 83566, propranolol, PGI2 or imidazole. Dopamine did not have any significant effect on the response to PGF2 alpha U-46619, KCl, 5-hydroxytryptamine or histamine.
D000818:Animals; D001011:Aorta / Q000502:physiology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology; D002396:Catechols / Q000494:pharmacology; D003345:Corticosterone / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology*; D004357:Drug Synergism; D006168:Guinea Pigs; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009637:Masoprocol; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology
D001095:Arachidonic Acids; D002396:Catechols; D016718:Arachidonic Acid; D009637:Masoprocol; D001241:Aspirin; D004298:Dopamine; D003345:Corticosterone; D009638:Norepinephrine; D007213:Indomethacin; D010646:Phentolamine