Effects of selective and nonselective beta-agonists on plasma potassium and norepinephrine.

The effects of graded infusions of the beta-agonists isoproterenol (nonselective), l-prenalterol (beta 1-selective), and salbutamol (beta 2-selective) on plasma potassium and norepinephrine were compared in subjects with borderline hypertension. Potassium levels fell with all three agonists, and norepinephrine levels rose with isoproterenol and salbutamol. These effects on potassium and norepinephrine were closely correlated and occurred at the same dose ranges as the cardiovascular responses. The fall in plasma potassium was probably caused by activation of beta-receptors, mainly on skeletal muscle, with subsequent stimulation of active sodium-potassium transport across the cellular membrane. The rise in plasma norepinephrine may have been due to activation of beta-receptors on sympathetic nerve endings. Activation of these presynaptic receptors is known to enhance the release of norepinephrine during nerve stimulation. For a given increase in heart rate and cardiac contractility, as measured by the heart rate-corrected duration of total electromechanical systole, which are mainly beta 1-responses, the effects on potassium and norepinephrine were in the order: salbutamol greater than isoproterenol greater than prenalterol. beta-Blockade with propranolol (nonselective), 80 mg four times a day, or atenolol (beta 1-selective), 100 mg once a day, antagonized the hypokalemic effect of isoproterenol as well as the rise in norepinephrine, but when isoproterenol was infused in doses high enough to overcome the blockade of the heart rate response, the effects on norepinephrine and potassium were abolished by propranolol and not by atenolol. Thus, the receptors in question appear to be of the beta 2-subtype.(ABSTRACT TRUNCATED AT 250 WORDS)