Effect of prostacyclin on cardiac transmembrane currents.
The relatively stable sodium salt of prostacyclin, PGI2-Na, kindly supplied by Chinoin Works (Budapest), was found to induce a dose-dependent increase in the inward-going membrane current of the sinoauricular fiber of the frog. Threshold concentration was 0.05 microgram/ml, and maximal effect was reached at a concentration of about 0.1 microgram/ml. Supramaximal concentrations of PGI2-Na evoked a maximal response, in contrast to primary prostaglandins, the dose-response curves of which decline at supramaximal values. The stimulatory effect of PGI2-Na was confined to the fast component of the inward current and was also readily demonstrable in the presence of Mn ions, i.e., with the slow channel blocked. The PGI2-Na was, however, ineffective in sodium-free medium (choline Ringer) or in the presence of 1 microgram/ml tetrodotoxin. Endogenous prostacyclin is likely to contribute to the regulation of cardiac cell membrane processes.
D000818:Animals; D004562:Electrocardiography; D004837:Epinephrine / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects*; D009200:Myocardial Contraction / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D011898:Ranidae; D012849:Sinoatrial Node / Q000187:drug effects; D013779:Tetrodotoxin / Q000494:pharmacology
D007473:Ion Channels; D011453:Prostaglandins; D013779:Tetrodotoxin; D011464:Epoprostenol; D004837:Epinephrine