Prostaglandin-mediated inhibition of noradrenaline release: its resistance to variations in rate of prostaglandine synthesis.
Isolated rabbit hearts were perfused according to Langendorff. The bilateral sympathetic nerve supply to the organ was stimulated at intervals, and the overflow of noradrenaline and of prostaglandins of the E series in the effluent was assayed, using fluorimetric and bioassay methods, respectively. The synthesis of prostaglandins in the organ was stimulated, either by perfusing the heart at a low pO2, or by infusing nicotinic acid. Hypoxia increased the coronary flow, provided the prostaglandin synthesis was not inhibited, probably as a consequence of hypoxia stimulation was however, unaffected by hypoxia. Nicotinic acid also stimulated prostaglandin formation, doubling the overflow of the lipid in response to nerve stimulation. In this series, too, the release of NA induced by nerve stimulation was unaffected by stimulation of prostaglandin synthesis. It is concluded that local variations in the rate of prostaglandin synthesis are unable to change the degree to which the release of sympathetic neurotransmitter is inhibited. Furthermore, it is suggested that the prostaglandin synthesis in rabbit heart takes place in compartments, separated functionally or morphologically.
D000818:Animals; D004558:Electric Stimulation; D005260:Female; D006321:Heart / Q000294:innervation*; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009539:Nicotinic Acids / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism*; D010477:Perfusion; D011458:Prostaglandins E / Q000096:biosynthesis / Q000502:physiology*; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000502:physiology*
D009539:Nicotinic Acids; D011458:Prostaglandins E; D009638:Norepinephrine