Ventrolateral medullary pressor area: site of hypotensive action of clonidine

Susan Punnen, Raymond Urbanski, Abbott J. Krieger, Hreday N. Sapru

Research output: Contribution to journalArticlepeer-review

113 Scopus citations

Abstract

Intravenous injections of clonidine produce an initial transient increase in blood pressure followed by a long-lasting hypotension and bradycardia. The initial pressor response is due to activation of vascular α1-adrenergic receptors while the hypotension and bradycardia are caused by the central actions of clonidine. Although, hypothalamus, nucleus tractus solitarius (NTS), ventrolateral medulla and the intermediolateral cell column of the thoracolumbar spinal cord (IML) have been implicated, the exact site of these actions of clonidine in the central nervous system is not established. The results of this investigation suggest that the pressor area in the ventrolateral medulla (VLPA) is the site of hypotensive and bradycardic actions of intravenously administered clonidine. This conclusion is based on the observation that microinjections of idazoxan, a specific α2-adrenergic receptor blocker, into the VLPA prevented and reversed the hypotension and bradycardia despite the fact that other proposed sites of these actions (NTS, hypothalamus and IML) were intact and accessible to intravenously administered clonidine.

Original languageEnglish (US)
Pages (from-to)336-346
Number of pages11
JournalBrain research
Volume422
Issue number2
DOIs
StatePublished - Oct 6 1987

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Keywords

  • Clonidine
  • Idazoxan
  • Pressor area
  • Spontaneously hypertensive rat
  • Ventrolateral medulla
  • Wistar-Kyoto rat
  • α-Adrenergic receptor

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