Endogenous opiates mediate cardiac sympathetic inhibition in response to a pressor stimulus in rabbits

Two different patterns of response to a pressor stimulus occurred in conscious rabbits. This difference was not apparent when a depressor stimulus was applied. At levels of mean arterial pressure exceeding 120 mmHg one group of animals exhibited a marked bradycardia which was due to sympathetic inhibition in addition to vagal activation, while this sympathetic component appeared to be lacking in the second group of animals. Naloxone (0.1 mg/kg i.v.) markedly reduced the sympathetic inhibition elicited by phenylephrine but had no significant effect on the reflex vagal stimulation. Naloxone thereby abolished the difference in sensitivity of baroreflex control of heart rate in response to a pressor stimulus between the two groups of rabbits. Naloxone did not influence the sensitivity of the reflex response to nitroprusside. Morphine (2 mg/kg) increased the vagal component of the baroreceptor reflex in response to a pressor stimulus and the sensitivity of the reflex response to nitroprusside in all the rabbits, and this was antagonized by naloxone (0.1 mg/kg). Morphine also potentiated and naloxone antagonized the bradycardic response at levels of MAP exceeding 120 mmHg, in those rabbits which appeared to lack the cardiac sympathetic inhibitory component of the reflex. The results show that endogenous and exogenous opiates can increase the reflex bradycardia in response to a pressor stimulus in the conscious rabbit. The difference in baroreflex sensitivity in different animals may result from their varying ability to activate endogenous opioid systems which depress cardiac sympathetic activity.