POSSIBLE ROLE OF AN ENDOGENOUS OPIATE IN THE CARDIOVASCULAR EFFECTS OF CENTRAL ALPHA ADRENOCEPTOR STIMULATION IN SPONTANEOUSLY HYPERTENSIVE RATS

  • 1 January 1980
    • journal article
    • research article
    • Vol. 214  (1) , 203-208
Abstract
In unanesthetized spontaneously hypertensive rats (SHR), naloxone (0.5-2 mg/kg i.p.) or naltrexone (2 mg/kg) inhibited the hypotension and bradycardia produced by clonidine (5-20 .mu.g/kg i.v.). Chronic treatment of SHR with clonidine (3 .times. 20 .mu.g/kg per day orally for 12 days) reduced blood pressure and heart rate and these effects were acutely reversed by a single injection of naloxone. Naloxone reversed the hypotension produced by a single injection of .alpha.-methyldopa (50-300 mg/kg i.p.). In pentobarbital-anesthetized SHR, the hypotension and bradycardia produced by 5 .mu.g/kg of clonidine were inhibited by naloxone (2 mg/kg) or by yohimbine (1 mg/kg i.p.). Morphine (0.33 mg/kg i.v.) 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 the effects were not influenced by naloxone. An opiodergic component may be involved in the antihypertensive action of central .alpha. adrenoceptor stimulants in SHR. A similar mechanism is absent or inactive in the normotensive Wistar Kyoto rats.