Potassium balance and ouabain binding sites in intact porcine hearts during isoproterenol infusion.
A pacing-induced tachycardia causes a net loss of K+ from the myocardium whereas adrenergic stimulation at constant heart rate will cause a net K+ accumulation. In the intact heart, isoproterenol (ISO) will, as expected, exert both effects, but the net result with regard to K+ balance is unknown. In the experiments on intact porcine hearts presented herein, a shunt from the coronary sinus to the right atrium allowed continuous monitoring of the myocardial K+ balance. ISO caused heart rate, dP/dt, and peak aortic flow to increase to a new steady state in less than 10 sec. There was an initial K+ loss lasting 1 min followed by a 10- to 15-times larger net uptake subsiding after 7 min. Overall, tissue K+ increased by 140.5 +/- 60.0 mumole/100 g, corresponding roughly to a 3 mM increase in intracellular concentration during ISO infusion. Ouabain binding sites determined in intact biopsies from the left ventricle remained unchanged. Thus, ISO has a biphasic effect on myocardial K+ balance, eventually causing a net increase of tissue K+ content probably unrelated to the inotropic effects. Direct stimulation of the Na+, K+-ATPase without changing the number of enzymes is possible.
D000818:Animals; D002304:Cardiac Pacing, Artificial; D005260:Female; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D007700:Kinetics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010042:Ouabain / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D011955:Receptors, Drug / Q000187:drug effects* / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase; D013552:Swine
D011955:Receptors, Drug; C028996:cardiac glycoside receptors; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D007545:Isoproterenol; D011188:Potassium