Drinking: a final common pathway?

Administration of either naloxone, an opioid antagonist (1 mg/kg i.p.), or clonidine, an alpha 2 adrenoceptor agonist (12 micrograms/kg i.p.), attenuated the dipsogenic responses of female rats to both angiotensin II (200 micrograms/kg s.c.) and isoproterenol (25 micrograms/kg s.c.). The effect of simultaneous administration of naloxone and clonidine at these submaximal doses was an additive attenuation of both angiotensin II- and isoproterenol-induced water intakes. The absence of a significant interaction between naloxone and clonidine to inhibit drinking suggests that they act by a similar mechanism. Yohimbine, an alpha 2 adrenoceptor antagonist (300 micrograms/kg i.p.), administered in combination with naloxone, reversed the antidipsogenic effect on angiotensin II-induced drinking. These results provide further support for a role for alpha 2-adrenoceptors in laboratory-induced drinking in rats, and suggest the possibility that the antidipsogenic effect of naloxone is related to alpha 2 adrenergic mechanisms. A model to support these observations is presented in which two separate pathways for the induction of drinking (osmoreceptor- and angiotensin II-induced) converge on a final common pathway. Since both naloxone and clonidine inhibit responses to stimulation of both pathways for drinking, these results suggest that their actions are likely to be at some point as yet undetermined on the final common pathway.