Myocardial potassium balance during adrenergic stimulation.
1) The primary receptor mechanism of catecholamine-induced myocardial potassium uptake is beta 1-adrenoceptor stimulation. Thus, K+ uptake seems to be a general effect of beta-adrenergic stimulation, dominated by beta 1-receptors in heart and by beta 2-receptors in skeletal muscle according to subtype preponderance in either tissue. In the myocardium there is also an effect of alpha 1-adrenoceptor stimulation which causes a significantly smaller uptake and requires higher catecholamine concentrations. 2) Both humoral and nervous adrenergic stimulation of the heart induce a significant potassium uptake which transiently reduces coronary sinus K+ concentration. It is likely that these changes affect cardiac functioning in vivo. During intense endogenous sympathetic activity and by high dose pharmacological interventions, the magnitude of change in coronary sinus concentration suggests that the reduction in extracellular K+ within the myocardium could be up to 1 mM. Under vulnerable conditions like hypokalemia and localized ischemia such changes might contribute to the risk for malignant arrhythmias. 3) Presumably net myocardial K+ accumulation is accompanied by a reciprocal reduction of intracellular Na+ concentration, which tends to reduce myocardial contractility and contribute to impaired cardiac function after a period of strong adrenergic stimulation. In vivo the negative inotropic effect could not be detected as long as catecholamines were supplied, but it occurred after stimulation was stopped. 4) In the intact beating heart beta-adrenergic stimulation increases Na,K-pumping 2.5 fold, from 15% of the maximum possible pump rate in control to 40% of maximum at high inotropy. These findings imply the presence of a substantial spare Na,K-pump capacity of the non-ischemic myocardium, even during intense sympathetic activity. Comparison of changes in pump rate and accumulated ionic shifts indicates that catecholamine-induced stimulation of Na,K-ATPase might be due to increased sensitivity for intracellular sodium.
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D000818:Animals; D002395:Catecholamines / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011941:Receptors, Adrenergic / Q000187:drug effects; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D013552:Swine; D013564:Sympathetic Nervous System / Q000502:physiology
D002395:Catecholamines; D011941:Receptors, Adrenergic; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D004837:Epinephrine