The role of beta1 and beta2 adrenoceptors in isoproterenol-induced drinking.

The present study examined the contribution of beta1 and beta2 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 beta1 adrenoceptors on the juxtaglomerular cells to release renin or by stimulating vascular beta2 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 beta1 adrenoceptor antagonist, or ICI 118,551 (1 mg/kg), a beta2 adrenoceptor antagonist, before treatment with isoproterenol (25 micrograms/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 beta1 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 beta1 and beta2 adrenoceptors by isoproterenol acts in a synergistic manner to induce drinking and renin-angiotensin system activation.