Opioid Peptides Mediate Sympathetic Inhibition in Response to Baroreceptor Activation in a Distinct Genetic Strain of Rabbit

Abstract

I . 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.2. 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 pg/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.3. Resting MAP and HR did not differ in the two groups. The mean gains of the cardiac baroreflex were 23.3 -t 2.2 ms/mmHg in Group I and 6.3 k I . 1 ms/mmHg in Group 11. After PE, MAP rose by 54.5 * 1.8 mmHg in Group I1 and 40.3 t 3.6 mmHg in Group I (Pt0.02). The pressor response was associated with a 3 I % reduction in plasma noradrenaline (NA) in Group I and a 34% increase in Group 11. The reduction in NA was significantly correlated with the degree of bradycardia in Group I (r=0.72, Pt0.05) and with BRS in both groups (r=0.78, PtO.01). Naloxone reduced BRS in Group I to 8.2 f 1.0 ms/mmHg and virtually abolished the fall in plasma NA in response to PE. 4. 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.

The role of cardiopulmonary baroreceptors during the forearm vasodilatation response to mental stress

“…Schobel, Oren, Mark, and Ferguson (1992) showed that the opioid antagonist naloxone selectively augments cardiopulmonary baroreflex regulation of sympathetic neural activity during lower body negative pressure from 0 to −15 mmHg in humans. Weinstock and Weksler‐Zangen (1989) have also shown that low baroreflex sensitivity was due to deficient opioid inhibition of sympathetic outflow in rabbits.…”

The Influence of Captopril and Naloxone on the Valsalva Manoeuvre and Systolic Time Intervals in Healthy Volunteers

“…The resulting arteriolar vasodilatation is however not accompanied by a reflex tachycardia (Shepherd et al 1982;Ajayi et al 1985a;Campbell et al 1985;West et al 1991). This may be due to either altered baroreceptor sensitivity (Warren et al 1983;Osterziel et al 1990;Smith et al 1991) baroreceptor resetting (West et al 1991) or alterations in the autonomic control of heart rate (HR) (Ajayi et al 1985a;Campbell et al 1985;Weinstock & Weksler-Zangen 1989;Fernandez et al 1990). Evidence for the presence of enkephalin in prevertebral sympathetic ganglia would support the latter explanation.…”