[Action of delta 9 tetrahydrocannabinol on the central cardiovascular regulation : mechanism and localization]

Delta9-tetrahydrocannabinol (30-300 mug.kg-1 i.v.) induced in cats and dogs a decrease in blood pressure and heart rate. This decrease appears to be centrally mediated. In fact, the splanchnic and cardiac discharges were reduced in intact animals as well as in debuffered cats ruling out a reflexly mediated action. The mechanism of this central decrease in the sympathetic tone appears to be different from the mechanism of the reduction induced by clonidine or by narcotic analgesics agents. In fact, piperoxan (1 mg.kg-1 i.v.), an alpha adrenoceptor blocking agent, antagonized or reversed the centrally mediated reduction in the sympathetic tone induced by clonidine or L-dopa, but did not change the effects of narcotic analgesic agents and of delta9-tetrahydrocannabinol. Naloxone (30 mug.kg-1 i.v.) prevented or reversed the cardiovascular effects of fentanyl and the reduction in splanchnic discharges induced by this agent, but no change was found after naloxone in the effects of clonidine or delta9-tetrahydrocannabinol. The pressor response to high frequency stimulation of the medulla oblongata was abolished by small doses of delta9-tetrahydrocannabinol. This agent did not reduce the pressor response to stimulation of the posterior hypothalamus induced by supramaximal stimulation and did not alter the hypertensive effect induced by stimulation of the cervical spinal cord. Medulla oblogata appears therefore to be the main site of action.