Wilkinson D L, Scroop G C
Clin Exp Pharmacol Physiol. 1986 Mar;13(3):179-86. doi: 10.1111/j.1440-1681.1986.tb00335.x.
In greyhounds anaesthetized with morphine and chloralose, vertebral artery infusions of angiotensin II resulted in a similar pressor response but smaller tachycardia than in greyhounds anaesthetized with chloralose alone. The pressor responses to intravenous infusions of angiotensin II were significantly larger in the morphine premedicated greyhounds. In greyhounds anaesthetized with morphine and chloralose, pressor responses to vertebral artery angiotensin II were potentiated following the administration of naloxone via either a vertebral artery or intravenously although the effect was more consistent with the former route. No such effect was seen in greyhounds anaesthetized with chloralose alone. Naloxone had no effect on the pressor responses to intravenous angiotensin II or carotid artery occlusion. The heart rate responses to vertebral artery angiotensin II in greyhounds anaesthetized with morphine and chloralose were potentiated by naloxone such that they were not significantly different from the responses obtained in greyhounds anaesthetized with chloralose alone before naloxone. As was observed with the pressor responses, the potentiation was more apparent with the vertebral artery route of administration of naloxone. There was no potentiation of the heart rate responses in the chloralose group of greyhounds. It is suggested that morphine premedication may repress the vagal withdrawal mechanism while potentiating the sympathetic vasomotor mechanism mediating the central cardiovascular actions of angiotensin II.