Stimulation of monovalent cation active transport by low concentrations of cardiac glycosides. Role of catecholamines.

The stimulatory effect of low concentrations of ouabain on the Na-K pump in isolated guinea pig left atria was studied in vitro by assessing active transport of the K(+) analog Rb(+). Active transport of Rb(+) was stimulated 20+/-8% (SEM, P < 0.05) above control values by 3 nM ouabain, but was inhibited by concentrations >10 nM. Preincubation with the beta-adrenergic antagonist propranolol (1 muM) completely blocked stimulation of active transport of Rb(+) by 3 nM ouabain. Norepinephrine, 10 nM, increased Rb(+) active transport 29+/-10% (P < 0.02) above control values. The beta-adrenergic agonist l-isoproterenol, 10 nM, increased active transport of Rb(+) by 33+/-10% (P < 0.01) above control levels. This stimulatory effect was abolished if tissues were first exposed to propranolol. Tyramine (0.1 muM), a stimulator of endogenous catecholamine release, increased active transport of Rb(+) 26+/-12% (P < 0.05) above control values. Rb(+) active transport was not significantly changed when left atrial tissues were incubated with alpha-adrenergic agonists or antagonists. Ouabain stimulation of Rb(+) active transport was prevented by in vivo depletion of myocardial endogenous catecholamines by either reserpine or 6-hydroxydopamine. These findings indicated that in myocardial tissue, Na-K pump stimulation by low concentrations of ouabain is mediated at least in part through beta-adrenergic effects of endogenous catecholamines.