ABSTRACT
1. In conscious rabbits the intravenous infusion of adrenaline (0.3 microgram kg-1 min-1), noradrenaline (1 microgram kg-1 min-1) or isoprenaline (1.25 micrograms kg-1 min-1) caused a significant decrease in plasma potassium levels. Propranolol (9 mg kg-1, s.c.) and ICI 118551 (30 micrograms kg-1, s.c.) reversed adrenaline-induced hypokalaemia and revealed a sustained hyperkalaemia. 2. Salbutamol (0.5 microgram kg-1 min-1, i.v.), beta 2-adrenoceptor agonist, evoked a biphasic response: an initial hyperkalaemia which was followed by a hypokalaemia; a higher dose (3 micrograms 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 beta 1-, beta 2- and beta 3-adrenoceptor antagonist, but not in the presence of the beta 1-adrenoceptor antagonist CGP 207 12A (1 mg kg-1, s.c.). 4. BRL 37344 (0.15 microgram kg-1 min-1, i.v.), SR 58611A (0.26 microgram kg-1 min-1, i.v.), both full beta 3-agonists, and CGP 12177 (0,25 micrograms kg-1 min-1, i.v.), a partial agonist which also acting as a non-selective beta 1- and beta 2-antagonist, induced a significant hypokalaemia. Bupranolol, but not ICI 118551 or CGP 20712A, blocked the BRL 37344-mediated hypokalaemia. 5. Ouabain (1.7 micrograms 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 beta 2- and beta 3-adrenoceptor control of extrarenal potassium disposal; moreover both beta 2 and beta 3 hypokalaemic effects would be mediated by activation of Na,K-pumps.
