EFFECTS OF SELECTIVE AND NONSELECTIVE BETA-AGONISTS ON PLASMA POTASSIUM AND NOREPINEPHRINE

  • 1 January 1984
    • journal article
    • research article
    • Vol. 6  (1) , 107-114
Abstract
The effects of graded infusions of the .beta.-agonists isoproterenol (nonselective), l-prenalterol (.beta.1-selective) and salbutamol (.beta.2-selective), on plasma K+ and norepinephrine were compared in subjects with borderline hypertension. K+ levels fell with all 3 agonists, and norepinephrine levels rose with isoproterenol and salbutamol. These effects on K+ and norepinephrine were closely correlated and occurred at the same dose ranges as the cardiovascular responses. The fall in plasma K+ was probably caused by activation of .beta.-receptors, mainly on skeletal muscle, with subsequent stimulation of active Na+-K+ transport across the cellular membrane. The rise in plasma norepinephrine may be due to activation of .beta.-receptors on sympathetic nerve endings. Activation of these presynaptic receptors enhances 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 K+ and norepinephrine were in the order: salbutamol > isoproterenol > prenalterol. .beta.-Blockade with propranolol (nonselective), 80 mg 4 times/day, or atenolol (.beta.1-selective), 100 mg once/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 K+ were abolished by propranolol and not by atenolol. The receptors in question appear to be of the .beta.2-subtype. Epinephrine, which circulates in high concentrations under stressful conditions, is generally considered to be the endogenous activator of these receptors. .beta.-Blockers may prevent hypokalemia and may suppres sympathetic activity, which could contribute to their so-called cardioprotective action. Evidently, .beta.2-type receptors are involved in stress-induced hypokalemia and in presynaptic facilitation of norepinephrine release.

This publication has 1 reference indexed in Scilit: