Potentiating effect of indomethacin on relaxations of sheep isolated coronary artery caused by sympathetic nerve stimulation or exogenous noradrenaline.
Indomethacin, 2.8 microM, potentiated relaxation responses of sheep, isolated, superfused coronary arteries caused by electrical transmural stimulation of sympathetic nerves by 2.3 fold, while responses to exogenous noradrenaline were not significantly altered. A ten fold higher concentration of indomethacin potentiated responses to sympathetic nerve stimulation by 3.4 fold and to exogenous noradrenaline by 1.8 fold. Stimulation-induced efflux of radioactivity derived from 3H-(-)-noradrenaline in sheep coronary arteries was not significantly altered by indomethacin (28 microM). Thus, while indomethacin-induced potentiation of relaxation responses to sympathetic nerve stimulation, was not due to an inhibition of prejunctional actions of prostaglandins, it may involve inhibition of the synthesis of prostaglandins which have post-junctional effects.
D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004558:Electric Stimulation; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology*; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology*; D012756:Sheep; D013564:Sympathetic Nervous System / Q000502:physiology*
D009638:Norepinephrine; D007213:Indomethacin