OPIOID PEPTIDES MEDIATE SYMPATHETIC INHIBITION IN RESPONSE TO BARORECEPTOR ACTIVATION IN A DISTINCT GENETIC STRAIN OF RABBIT

Two strains of rabbits have been bred with marked differences in their cardiac baroreflex sensitivity (BRS). The difference in cardiac BRS was attenuated by naloxone. We compared the sympathetic responses to a pressor stimulus in these two strains, by measuring the changes in plasma catecholamines in the presence and absence of naloxone. Cardiac BRS was assessed in eight rabbits of each group by the steady‐state method. Two weeks later, both ear arteries and one ear vein were cannulated. Mean arterial pressure (MAP) and heart rate (HR) were recorded from one artery and blood samples (5 mL) for plasma catecholamines (CA) taken before, and during the peak of the pressor response to intravenous phenylephrine (PE, 20 ug/kg) from the other. The experiment was repeated 2‐3 weeks later in rabbits with high BRS (Group I) after injection of naloxone 0.1 mg/kg, i.v. Resting MAP and HR did not differ in the two groups. The mean gains of the cardiac baroreflex were 23.3 ± 2.2 ms/mmHg in Group I and 6.3 ± 1.1 ms/mmHg in Group II. After PE, MAP rose by 54.5 ± 1.8 mmHg in Group II and 40.3 ± 3.6 mmHg in Group I P<0.02. The pressor response was associated with a 31 % reduction in plasma noradrenaline (NA) in Group I and a 34% increase in Group II. The reduction in NA was significantly correlated with the degree of bradycardia in Group I (r = 0.72, P<0.05) and with BRS in both groups (r = 0.78, P<0.01). Naloxone reduced BRS in Group I to 8.2 ± 1.0 ms/mmHg and virtually abolished the fall in plasma NA in response to PE. We suggest that stimulation of cardiopulmonary afferents by a strong pressor stimulus in Group I rabbits results in sympathetic inhibition which involves the mediation of opioid peptides.