The present study examined the contribution of beta(1) and beta(2) adr
enoceptor activation to drinking behavior and the stimulation of plasm
a renin activity produced by the mixed beta adrenoceptor agonist, isop
roterenol. The stimulation of drinking by beta adrenoceptor activation
could occur via two independent pathways; by either directly stimulat
ing renal beta(1) adrenoceptors on the juxtaglomerular cells to releas
e renin or by stimulating vascular beta(2) adrenoceptors that would de
crease blood pressure and activate afferent neural and humoral mechani
sms. Selective pharmacological antagonism of each adrenoceptor type wa
s achieved by administering atenolol (2.5 mg/kg), a beta(1) adrenocept
or antagonist, or ICI 118,551 (1 mg/kg), a beta(2) adrenoceptor antago
nist, before treatment with isoproterenol (25 mu g/kg). Neither adreno
ceptor mechanism alone could account for all of the water intake or st
imulation of plasma renin activity due to isoproterenol treatment. Car
diovascular 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 th
e beta(2) adrenoceptor-mediated depressor response to isoproterenol. T
he results provide evidence that the stimulation of both beta(2) and b
eta(2) adrenoceptors by isoproterenol acts in a synergistic manner to
induce drinking and renin-angiotensin system activation.