COEXISTENCE OF BETA-2-ADRENOCEPTOR AND BETA-3-ADRENOCEPTOR IN PLASMA POTASSIUM CONTROL IN CONSCIOUS RABBITS

1 In conscious rabbits the intravenous infusion of adrenaline (0.3 mug kg-1 min-1), noradrenaline (1 mug kg-1 min-1) or isoprenaline (1.25 mug kg-1 min-1) caused a significant decrease in plasma potassium levels. Propranolol (9 mg kg-1, s.c.) and ICI 118551 (30 mug kg-1, s.c.) reversed adrenaline-induced hypokalaemia and revealed a sustained hyperkalaemia. 2 Salbutamol (0.5 mug kg-1 min-1, i.v.), beta2-adrenoceptor agonist, evoked a biphasic response: an initial hyperkalaemia which was followed by a hypokalaemia; a higher dose (3 mug kg-1 min-1, i.v.) solely induced hypokalaemia. ICI 118551 blocked the salbutamol-mediated response. 3 Noradrenaline evoked hypokalaemia was blunted completely in the presence of bupranolol (0.1 mg kg-1, s.c.), a beta1-, beta2- and beta3-adrenoceptor antagonist, but not in the presence of the beta1-adrenoceptor antagonist CGP 20712A (1 mg kg-1, s.c.). 4 BRL 37344 (0.15 mug kg-1 min-1, i.v.), SR 58611A (0.26 mug kg-1 min-1, i.v.), both full,83-agonists, and CGP 12177 (0,25 mug kg-1 min-1, i.v.), a partial agonist which also acting as a non-selective beta1- and beta2-antagonist, induced a significant hypokalaemia. Bupranolol, but not ICI 118551 or CGP 20712A, blocked the BRL 37344-mediated hypokalaemia. 5 Ouabain (1.7 mug kg-1 min-1, i.v.), an inhibitor of the Na,K-pumps, inhibited both salbutamol-and BRL 37344-mediated hypokalaemia. 6 These data suggest the coexistence of beta2- and beta3-adrenoceptor control of extrarenal potassium disposal; moreover both beta2 and beta3 hypokalaemic effects would be mediated by activation of Na,K-pumps.