Transmembrane action potentials were recorded from isolated electrically paced cat and guinea pig left auricles in Tyrode solution and in the presence of 25 mM K+ or tetrodotoxin (TTX). The overshoot (OS) was increased, and the plateau of the action potential (AP) was shortened by epinephrine (5 X 10(-6)M) and by celluline-A (an organic calcium complex obtained from frog skin). The maximum rate of depolarization (Vmax) was enhanced by serotonin (5-HT) (10(-6)M), prostaglandin F2 alpha (2.8 X 10(-6)M), and by celluline-A. After inactivation of the fast sodium channel by TTX (10(-5)M) or by partial depolarization (25 mM K+ Tyrode) of electrically driven cat and guinea pig left auricle, catecholamines (epinephrine and isoproterenol, 4 X 10(-7) to 5 X 10(-6)M), histamine (10(-6) to 10(-5)M), and celluline-A restored the electrical and mechanical activity. Prostaglandins (PGE1, PGF2 alpha, 1.4 X 10(-8)-2.8 X 10(-6)M), 5-HT (10(-6)-5 X 10(-6)M), and 4-aminopyridine (1.5 X 10(-4)M) were ineffective in such conditions. The beta-adrenergic blocking agent pindolol (4 X 10(-7)M) prevented only the effect of catecholamines; the H1 receptor blocker mepyramine (10(-5)M) antagonized only that of histamine, and D-600 (2 X 10(-6)M), a selective Ca channel blocker, prevented the restoring effect of catecholamines, histamine, and celluline-A.
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