Catecholamine-induced myocardial potassium uptake mediated by beta 1-adrenoceptors and adenylate cyclase activation in the pig.

The myocardial potassium uptake during intracoronary isoproterenol stimulation was characterized in 12 anesthetized pigs. The beta-receptor subtype specificity and the effect of adenylate cyclase activation were determined. Potassium concentrations were continuously recorded by PVC-valinomycin minielectrodes in the left atrial cavity and in coronary sinus blood diverted through a shunt to the right atrium. The difference in potassium concentration between the left atrial cavity and coronary sinus, and the accumulated myocardial potassium uptake were calculated after computerized data sampling. By intracoronary drug infusion, changes in heart rate and systemic effects were minimized. Isoproterenol (0.6-0.8 microgram/min), a nonspecific beta-agonist, reduced coronary sinus potassium concentration transiently to a nadir of 0.28 (0.15-0.43) mM (median and 95% confidence interval) below control values (n = 12). The potassium uptake, which amounted to 140 (79-202) mumol/100 g tissue, corresponding to an intracellular potassium increase of about 3 mM, was abolished after selective beta 1-blockade by pafenolol. The specific beta 1-agonist dobutamine (40 micrograms/min) caused a similar potassium uptake before and after selective beta 2-blockade by ICI 118, 551. Salbutamol (2 micrograms/min), a specific beta 2-agonist, induced a minor potassium uptake of 4 (1-20) mumol/100 g, blocked by pafenolol. After nonselective beta-blockade by propranolol the adenylate cyclase stimulator forskolin caused a myocardial potassium uptake of similar magnitude to that of isoproterenol before beta-blockade. We conclude that a myocardial potassium uptake ensues during beta 1-adrenoceptor stimulation and adenylate cyclase activation.