The effects of intracerebroventricular (i.c.v.) and intracisternal (i.c.) injection of beta-endorphin on arterial blood pressure (BP) in rats that received five intraperitoneal injections of monosodium glutamate (MSG) on alternate days in the first 10 days of life were studied. 2. beta-endorphin administered into the lateral ventricles caused a prolonged elevation in BP, whereas i.c. injection of the peptide resulted in an even longer lasting reduction in BP. In the MSG-treated rat, the prolonged hypertensive effect of i.c.v. injection of beta-endorphin was completely abolished, but the effect of i.c. injection of the peptide was the same as that in the control. Since MSG treatment destroyed selectively the structures around the third ventricle, it is suggested that these structures, including the arcuate nucleus, may be responsible for mediating the cardiovascular effects of beta-endorphin. 3. The effects of central administration of beta-endorphin were completely blocked by naloxone, which mainly antagonizes the actions of mu-receptor agonists and has no cardiovascular effects itself. The results suggest that mu-receptors may be involved in mediation of the effects of beta-endorphin on the cardiovascular system and that beta-endorphin in the brain may not exert a tonic influence on the cardiovascular functions.
