Beta-Adrenergic modulation of Ba2+ currents and K+ contractures in frog slow skeletal muscle fibers.

Abstract

beta-Adrenergic modulation of the Ba2+ current (IBa) and K+ contracture in slow skeletal muscle fibers of the frog (Rana pipiens) were investigated in intact fibers with the three-microelectrode voltage-clamp technique and isometric tension measurements. Application of epinephrine (10(-6) to 10(-5) M) to the bath increased the amplitude of IBa. This increase was blocked by the beta-antagonist propranolol (3 microM), and a similar increase was observed with the beta-specific agonist isoproterenol (1 microM). Thus the epinephrine effect was mediated mainly by beta-adrenergic receptors. External application of permeable 8-bromoadenosine 3',5'-cyclic monophosphate (0.5 mM) increased the amplitude of both IBa and K+ contractures. The present results suggest that beta-adrenergic modulation of IBa in slow skeletal muscle fibers could reflect a modulation of Ca2+ channels via adenosine 3',5'-cyclic monophosphate (cAMP). cAMP (0.5 mM) also potentiated the K(+)-evoked tension in these slow fibers. The physiological contribution made by the modulation of slow skeletal muscle Ca2+ channels to the increase in tension is still not completely understood.