ALPHA(1B)-ADRENOCEPTOR-MEDIATED STIMULATION OF NA-K PUMP CURRENT IN ADULT-RAT VENTRICULAR MYOCYTES

The purpose of this study was to determine if myocardial alpha1a- and/ or alpha1b-adrenoceptors are involved in the increase in Na-K pump cur rent (I(p)) elicited by alpha1-adrenergic agonists. Single rat ventric ular myocytes were isolated by enzymatic disaggregation. The whole cel l patch-clamp technique was used to examine dose-dependent effects of phenylephrine (PE) on holding current (I(h)) and to determine whether observed actions were mediated via alpha1a- or alpha1b-adrenergic rece ptors. To minimize the contribution of transsarcolemmal currents other than I(p) to I(h), membrane voltage was held constant at -40 mV, and cells were maintained in a Ca-free perfusate containing 1 mM Ba and 0. 1 mM Cd. All experiments were conducted in the presence of 3 muM nadol ol. PE elicited dose-dependent increases in I(h), with a peak effect o f 0.57 +/- 0.03 pA/pF observed at 30 muM. The response to PE was dose dependently inhibited by prazosin and chloroethylclonidine and was tot ally eliminated by 1 mM ouabain. When used at doses selective for the alpha1a-subtype, WB4101 failed to significantly antagonize the action of PE. These data suggest that the observed alpha1-adrenoceptor-mediat ed increase in I(h) in isolated rat ventricular myocytes is the result of an increase in I(p) effected via stimulation Of alpha1b-adrenergic receptors.