Stimulation of Monovalent Cation Active Transport by Low Concentrations of Cardiac Glycosides: <i>ROLE OF CATECHOLAMINES</i>

Thomas J. Hougen; Nancy Spicer; Thomas W. Smith

doi:10.1172/JCI110366

Stimulation of Monovalent Cation Active Transport by Low Concentrations of Cardiac Glycosides: ROLE OF CATECHOLAMINES

Thomas J. Hougen, Nancy Spicer, and Thomas W. Smith

Published November 1, 1981 - More info

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Abstract

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 β-adrenergic antagonist propranolol (1 μM) 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 β-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 μM), 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 α-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 β-adrenergic effects of endogenous catecholamines.