Fregly M J, Rowland N E, Greenleaf J E
Brain Res Bull. 1984 Apr;12(4):393-8. doi: 10.1016/0361-9230(84)90111-4.
Studies from this laboratory have shown that either central or peripheral administration of clonidine, the alpha 2-adrenoceptor agonist, can attenuate a variety of dipsogenic stimuli in rats. Further, yohimbine and tolazoline, alpha 2-adrenoceptor antagonists, augment the drinking response to both peripherally administered isoproterenol and angiotensin II. Studies reported here establish a dose-inhibition relationship between the dose of clonidine administered (2 to 32 micrograms/kg) intracerebroventricularly (IVT) and inhibition of the drinking response to peripherally administered angiotensin II (200 micrograms/kg. SC). DI50 was approximately 4 micrograms/kg. Yohimbine (300 micrograms/kg, SC) reversed the antidipsogenic effect of centrally administered clonidine (32 micrograms/kg, IVT) on angiotensin II-induced (200 micrograms/kg, SC) water intake. Phenylephrine, an alpha 2-adrenoceptor agonist, administered IVT (40 and 80 micrograms/kg) also inhibited angiotensin II-induced drinking in a dose-related fashion. The antidipsogenic effect of phenylephrine (80 micrograms/kg) was blocked by administration of yohimbine (300 micrograms/kg. SC). Thus, this effect of phenylephrine most likely occurs by way of alpha 2-adrenoceptors. These results support a role for the pre-synaptic alpha 2-adrenoceptor in the mediation of drinking in rats. Activation of alpha 2-adrenoceptors is accompanied by reduced water intake while inhibition of these receptors enhances water intake.