Chronic nucleus tractus solitarius lesions do not prevent hypovolemia- induced vasopressin secretion in rats

A. M. Schreihofer, E. M. Stricker, A. F. Sved

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage 14 samples of 2 ml/300 g body wt taken every 10 mm increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats. SAD rats and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in α-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.

Original languageEnglish
Pages (from-to)R965-R973
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume267
Issue number4 36-4
DOIs
StatePublished - 1994

Keywords

  • arterial pressure
  • baroreceptors
  • heart rate
  • hemorrhage
  • polyethylene glycol
  • sinoaortic denervation
  • vagus

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