Blood Pressure and Splanchnic Nerve Activity Are Reduced by a Vagally Mediated Opioid Action

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Abstract
An enkephalin analogue. D-Ala2-Met3-enkephalinamide (DAME), caused a fall in blood pressure (BP) following right atrial administration (RA) in urethane-anesthetized rats that were also atropinized, paralyzed, and artificially ventilated. This reduction in BP was not related to opioid-induced bradycardia. At a dose of 250 μg/kg RA the maximum percentage change was −36.0 ± 3.9% occurring within 10–15 s subsequent to administration. The fall in BP was blocked by both pretreatment with naloxone HCI (75–100 μg/kgiv.) and bilateral cervical vagotomy. Similar hypotensive responses (−37.3 ± 2.3%) were obtained with phenyldiguanide (PDG) (40 μg/kgRA), a known stimulant of pulmonary J receptors (pulmonary C fibers). However, unlike DAME, the PDG response could not be blocked by naloxone. The fall in BP, obtained with DAME and PDG, paralleled a reduction in the spike frequency of the greater splanchnic nerve activity. This reflex fall in activity, did not involve supramesencephalic structures because results were similar in both urethaneanesthetized and unanesthetized midcollicular decerebrate preparations. It was concluded that opioids can act peripherally, via pulmonary opiate receptors, to inhibit central vasomotor activity and reduce BP by eliciting a pulmonary chemoreflex.

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