Propranolol modifies myocardial Na+, K+-ATPase activity and increases its sensitivity to digitalis inhibition via a direct nonspecific membrane effect rather than an adrenergic mechanism.
May suggest enhanced digitalis effects with propranolol; leaves open clinical relevance pending human data.
It has been documented that biogenic amines can stimulate Na+, K+-ATPase from various tissue preparations. However, it is unclear whether or not this stimulation occurs in myocardial tissues. We have evaluated possible catecholamine stimulation of purified Na+, K+- ATPase preparations utilizing a bovine ventricular microsomal preparation. We have studied the dose response of the enzyme to ouabain and digitoxigenin in the presence and absence of propranolol and norepinephrine. Our results indicate that propranolol increases the sensitivity of Na+, K+-ATPase to inhibition by digitalis, and that stimulation of Na+, K+-ATPase in bovine myocardium is not mediated via an adrenergic mechanism. In addition, our results indicate that in myocardial tissue, both stereoisomers of propranolol produce a direct nonspecific membrane effect which can modify Na+, K+-ATPase activity.
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Cook et al. (1983) studied this question.
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