Cardiovascular effects of opioid antagonist naloxone in rostral ventrolateral medulla of rabbits

D. A. Morilak, G. Drolet, J. Chalmers

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opioid antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 ± 2 mmHg). This was preceded by a brief and mild depressor effect (-9 ± 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (-29 ± 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.

Original languageEnglish (US)
Pages (from-to)R325-R331
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume258
Issue number2 27-2
DOIs
StatePublished - 1990
Externally publishedYes

Keywords

  • aortic depressor nerve
  • arterial pressure
  • baroreflexes
  • central cardiovascular regulation
  • enkephalin
  • hemorrhage

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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