Elsner D, Kromer E P, Riegger A J
Medizinische Universitäts-Klinik, Würzburg, Federal Republic of Germany.
J Cardiovasc Pharmacol. 1989 Mar;13(3):376-81. doi: 10.1097/00005344-198903000-00004.
In intact anesthetized dogs, we measured myocardial potassium uptake, as calculated from the aortocoronary sinus difference in potassium concentration and myocardial blood flow, before and during beta-adrenergic stimulation with isoproterenol. Isoproterenol (10 and 30 ng/kg/min, n = 16) lowered arterial potassium concentration from 3.48 +/- 0.08 mmol/L by 0.20 +/- 0.07 and 0.32 +/- 0.06 mmol/L, coronary sinus potassium from 3.45 +/- 0.08 mmol/L by 0.20 +/- 0.06 and 0.35 +/- 0.06 mmol/L, increasing/myocardial potassium uptake from 1.94 +/- 0.99 mumol/min to 2.33 +/- 0.97 and 5.36 +/- 1.29 mumol/min. Unselective beta blockade (propranolol 0.1 mg/kg) significantly attenuated the fall in arterial and coronary sinus serum potassium and the increase in myocardial potassium uptake. Selective beta 1 blockade (metoprolol 0.1 mg/kg) did not significantly influence these effects. We conclude that beta-adrenergic stimulation increases myocardial potassium uptake, lowering serum potassium in the coronary bed, in addition to causing a systemic hypokalemia. This effect is mediated predominantly by beta 2 adrenoceptors.