Modulation by prostaglandins of the release of [3H] noradrenaline evoked by potassium and nerve stimulation in the isolated rat heart.
In the isolated rat heart perfused with Krebs solution and prelabeled with [3H] noradrenaline, we examined the effect of prostaglandins (PG) I2, E2, 6-keto-PGF1 alpha and their precursor, arachidonic acid, on the overflow of tritium elicited by potassium (K+) and by stimulation of cardiac sympathetic nerve plexus. Prostaglandins E2, I2 and arachidonic acid but not 6-keto-PGF1 alpha reduced K+ and nerve stimulation-induced overflow of tritium. Administration of indomethacin, an inhibitor of cyclooxygenase, increased tritium overflow elicited by either K+ or by nerve stimulation. During infusion of indomethacin, the inhibitory effect of both PGE2 and PGI2 on the K+ or nerve stimulation-induced overflow of tritium remained unaltered. In contrast, the effect of arachidonic acid to reduce K+ or nerve stimulation-induced overflow of tritium was abolished by indomethacin, indicating that the fatty acid inhibits release of tritium by its conversion to a product(s) of cyclooxygenase, presumably PGI2 and PGE2. These data suggest that prostaglandins, particularly PGI2 and PGE2 synthesized in the isolated rat heart act on prejunctional sites to modulate release of the adrenergic transmitter.
D000818:Animals; D004558:Electric Stimulation; D006321:Heart / Q000294:innervation; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*; D011453:Prostaglandins / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D013564:Sympathetic Nervous System / Q000502:physiology*
D011453:Prostaglandins; D011188:Potassium; D009638:Norepinephrine