Autonomic Regulation of a Chloride Current in Heart

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Abstract
In isolated heart cells, beta-adrenergic receptor stimulation induced a background current that was suppressed by simultaneous muscarinic receptor stimulation. Direct activation of adenylate cyclase with forskolin also elicited this current, suggesting regulation by adenosine 3',5'-monophosphate (cAMP). This current could be recorded when sodium, calcium, and potassium currents were eliminated by channel antagonists or by ion substitution. Alteration of the chloride equilibrium potential produced changes in the reversal potential expected for a chloride current. Activation of this chloride current modulated action potential duration and altered the resting membrane potential in a chloride gradient-dependent manner.