Antagonistic effect of naloxone on the hypertensive response of intraventricularly administered histamine

Intracerebroventricular (i.c.v.) injections of histamine (HA) to Vetbutal-anaesthetized rats elicited a biphasic pressor response: a fall of blood pressure (BP) in the first minute, followed by a rise in BP. The heart rate (HR) response was also biphasic: bradycardia in the first minute, followed by tachycardia. The H₁-receptor agonist 2-pyridylethylamine (PEA) increased the fall in BP in the first minute in comparison with the HA group, and then elicited a rise in BP that was, however, much lower than that produced by HA. Throughout the experiment PEA produced essentially only a bradycardia. The H₂-receptor agonist dimaprit elicited a single-phase pressor response, i.e. a rise in BP and did not elicit tachycardia. Intraventricular pretreatment of rats with naloxone greatly reduced the initial response (phase 1) in the first minute in HA groups by 77–83% and PEA groups by 83–100%. Naloxone given in small doses also reduced the fall in HR by 71–100% in those groups. The experimental results permit a conclusion that the phase 1 response, i.e. the fall in BP, results from excitation of H₁-receptors. Thus we may propose that H₁-receptors are involved in the action of naloxone. Naloxone in a dose of 0.1 g inhibited the hypertensive responses of HA after 25–30 min. The reduction reached 71%. Naloxone reduced the small rise in BP induced by PEA (10 g) but totally blocked the rise in BP induced by dimaprit (50 g). This blockade indicates that the central opioid system may transmit the total stimulating response (rise in BP) of H₂ receptors induced by dimaprit. Participation of central opioid receptors in HA-stimulated responses has already been demonstrated in corticosterone secretion 1].The study was supported by the Polish Academy of Sciences, grant No. 06.03.