THE ROLE OF BETA(1) AND BETA(2) ADRENOCEPTORS IN ISOPROTERENOL-INDUCED DRINKING

The present study examined the contribution of beta(1) and beta(2) adrenoceptor activation to drinking behavior and the stimulation of plasma renin activity produced by the mixed beta adrenoceptor agonist, isoproterenol. The stimulation of drinking by beta adrenoceptor activation could occur via two independent pathways; by either directly stimulating renal beta(1) adrenoceptors on the juxtaglomerular cells to release renin or by stimulating vascular beta(2) adrenoceptors that would decrease blood pressure and activate afferent neural and humoral mechanisms. Selective pharmacological antagonism of each adrenoceptor type was achieved by administering atenolol (2.5 mg/kg), a beta(1) adrenoceptor antagonist, or ICI 118,551 (1 mg/kg), a beta(2) adrenoceptor antagonist, before treatment with isoproterenol (25 mu g/kg). Neither adrenoceptor mechanism alone could account for all of the water intake or stimulation of plasma renin activity due to isoproterenol treatment. Cardiovascular recordings confirmed the selectivity of the antagonists to their respective receptor subtypes, with atenolol blocking the beta, adrenoceptor-mediated heart rate increases and ICI 118,551 blocking the beta(2) adrenoceptor-mediated depressor response to isoproterenol. The results provide evidence that the stimulation of both beta(2) and beta(2) adrenoceptors by isoproterenol acts in a synergistic manner to induce drinking and renin-angiotensin system activation.