RT Journal Article SR Electronic T1 Possible role of an endogenous opiate in the cardiovascular effects of central alpha adrenoceptor stimulation in spontaneously hypertensive rats. JF Journal of Pharmacology and Experimental Therapeutics JO J Pharmacol Exp Ther FD American Society for Pharmacology and Experimental Therapeutics SP 203 OP 208 VO 214 IS 1 A1 Farsang, C A1 Ramirez-Gonzalez, M D A1 Mucci, L A1 Kunos, G YR 1980 UL http://jpet.aspetjournals.org/content/214/1/203.abstract AB In unanesthetized sponatneously hypertensive rats (SHR), naloxone (0.5--2 mg/kg ip.) or naltrexone (2 mg/kg) inhibited the hypotension and bradycardia produced by clonidine (5--20 micrograms/kg iv.). Chronic treatment of SHR with clonidine (3 x 20 micrograms/kg/day orally for 12 days) reduced blood pressure and heart rate and these effects were acutely reversed by a single injection of naloxone. Naloxone also reversed the hypotension produced by a single injection of alpha-methyldopa (50--300 mg/kg ip.). In pentobarbital-anesthetized SHR, the hypotension and bradycardia produced by 5 micrograms/kg of clonidine were inhibited either by naloxone (2 mg/kg) or by yohimbine (1 mg/kg ip.). Morphine (0.33 mg/kg iv.) also reduced blood pressure and heart rate in these animals but these effects were only antagonized by naloxone and not by yohimbine. In conscious and anesthetized normotensive Wistar Kyoto rats, the reduction in blood pressure and heart rate by clonidine or alpha-methyldopa were smaller than in SHR, and these effects were not influenced by naloxone. These results confirm and extend earlier observations and suggest the existence of an "opioidergic" component in the antihypertensive action of central alpha adrenoceptor stimulants in SHR. They also show that a similar mechanism is either absent or inactive in the normotensive Wistar Kyoto rats.