Origin of the hypotensive and sympathoinhibitory effect of morphinomimetic agents.

In vagotomized dogs, lesions of the lateral reticular nucleus (LRN) region did not change arterial blood pressure and sympathetic nerve activity. The hypertensive and tachycardic responses elicited by section of both carotid sinus nerves and both vagus nerves were not altered. However the sympathoinhibitory component of the baroreflex arc was attenuated. These lesions also abolished the hypotensive and sympathoinhibitory effects of fentanyl (10 micrograms/kg i.v.). In debuffered dogs, bilateral lesions of the LRN regions attenuated the effects of fentanyl (20 micrograms/kg i.v.) on arterial blood pressure and splanchnic discharges. Microinfusion of naloxone into the LRN reduced the effects of fentanyl (10 micrograms/kg) administered intravenously. Microinfusion of [D-Ala2,Met5]enkephalinamide (0.1-1 microgram) into the LRN region produced a dose dependent decrease in arterial blood pressure and sympathetic nerve activity. Lesions of the nucleus ambiguus (NA) region also reduced the effects of fentanyl. In contrast, lesions placed in the ventral median reticular formation or above the NA were ineffective in changing the sympathoinhibitory effect of fentanyl. These results indicate that the lateral reticular formation ventral to the nucleus ambiguus including the lateral reticular nucleus region is involved in the sympathoinhibitory effect of morphinomimetic agents.