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beta-endorphin acting on the brainstem is involved in the antihypertensive action of clonidine and alpha-methyldopa in rats.

The possible involvement of 0-endorphin in the antihypertensive action of clonidine and a-methyldopa, drugs acting on central a2-adrenergic receptors, has been examined in rats with spontaneous, steroid-salt, or one-kidney, one-clip renal hypertension. In all three groups of rats, the hypotensive effect of a single intraperitoneal injection of 100 mg/kg of a-methyldopa was partially reversed by naloxone (2 mg/kg, ip) or reduced by pretreatment with naltrexone (2 mg/kg, ip). In matched normotensive control rats, a-methyldopa caused a slight reduction or no change in blood pressure, and subsequently administered naloxone had no significant effect on blood pressure. Administration of an antiserum to j3-endorphin into the 4th cerebral ventricle of awake rats inhibited the hypotension and bradycardia produced by intravenous or intracerebroventricular injection of clonidine in all three groups of hypertensive animals. Intracerebroventricular injection of /9-endorphin caused hypotension and bradycardia in spontaneously hypertensive rats. Baroreflex sensitivity was assessed in normotensive Wistar-Kyoto rats and in spontaneously hypertensive rats from the bradycardic response to systemic administration of graded doses of phenylephrine. Naltrexone, 2 mg/kg, ip, did not influence baroreflex sensitivity in Wistar-Kyoto rats but increased it in spontaneously hypertensive rats, as indicated by a progressively greater bradycardia in response to increasing pressure rise. It is concluded that /S-endorphin acting on opiate receptors in the brainstem is involved in the antihypertensive action of central a2-adrenergic receptor activation, that the absence of this mechanism in normotensive animals and its presence in animals with different forms of hypertension indicates that it is activated by the hypertensive process itself, and that this depressor endorphinergic system is distinct from and its effects are opposite to those of other endogenous opioids that appear to tonically inhibit baroreflex sensitivity in spontaneously hypertensive rats. (Circ Res 53: 150-157, 1983)