Effects of peripheral administration of naloxone on beta-adrenergic mediated responses

A possible interaction between the opiate and beta-adrenergic systems in controlling body temperature, heart rate and water intake was investigated using adult male Sprague-Dawley rats. Peripheral administration of isoproterenol (8 and 50 micrograms/kg, s.c.) produced significant elevations of heart rate and tail skin and colonic temperatures, respectively. Peripheral pretreatment with naloxone (1 mg/kg, s.c.) was without effect on these beta-adrenergic responses. Administration of isoproterenol (25 micrograms/kg, s.c.) produced a significant increase in water intake which was abolished by peripheral pretreatment with naloxone (1 mg/kg, s.c.). Previous studies have suggested that the dipsogenic response to isoproterenol is mediated through angiotensin II. In the present study the angiotensin II-induced (200 micrograms/kg, s.c.) dipsogenic response was abolished by naloxone pretreatment. However, pretreatment with an equimolar dose of naloxone methobromide, an opiate antagonist which does not cross the blood-brain barrier, was ineffective in altering the dipsogenic response produced by peripheral administration of either angiotensin II or isoproterenol. Collectively, the data suggest that opiates do not alter peripheral beta-adrenergic responses and that the blocking effects of naloxone on the isoproterenol-induced drinking response is mediated centrally and may be due to blocking angiotensin II dipsogenesis.