Augmentation of isoproterenol-induced drinking by acute treatment with certain dopaminergic agonists.

Bromocriptine (1 mg/kg, IP), a dopaminergic agonist that crosses the blood-brain barrier, augmented the dipsogenic responsiveness of rats to acute administration of the beta-adrenergic agonist, isoproterenol (15 micrograms/kg, SC), when administered at the same time. When administered alone, it had no effect on either water intake or urine output. Dopamine (20 mg/kg IP), which does not cross the blood-brain barrier, also augmented the dipsogenic responsiveness to acute administration of isoproterenol. However, a major difference between the responses to bromocriptine and dopamine was that the latter augmented drinking only when administered 15 to 30 min prior to isoproterenol. During the 30 min between injection of dopamine and the injection of isoproterenol, output of urine and sodium increased approximately 6-fold above the level of controls such that the concentration of the urine excreted by the treated group was approximately isotonic. However, in spite of a 6-fold increase in output of urine by the treated, compared to the control group, dopamine-treated rats ingested water only to the same extent as untreated controls when access to water was allowed. This suggests that an isotonic contraction of extracellular fluid may not induce a dipsogenesis. It also suggests that the augmentation of isoproterenol-induced drinking by dopamine was not the result of a dehydration-induced drink superimposed on the isoproterenol-induced drink. The centrally and peripherally acting dopaminergic antagonist, spiroperidol (spiperone), inhibited the isoproterenol-induced drinking response in a dose-related fashion. However, the peripherally acting dopaminergic antagonist, domperidone,was without effect on isoproterenol induced drinking.(ABSTRACT TRUNCATED AT 250 WORDS)