Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

Nitric oxide is not involved in the control of vasopressin release during acute forced swimming in rats

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Engelmann, M.
  • Wolf, G.
  • Putzke, J.
  • Bloom, Floyd
  • Raber, J.
  • Landgraf, R.
  • Spina, M. G.
  • Horn, T. F. W.

publication date

  • February 2004

journal

  • Amino Acids  Journal

abstract

  • Neurons of the hypothalamo-neurohypophyseal system (HNS) are known to contain high amounts of neuronal nitric oxide (NO) synthase (nNOS). NO produced by those neurons is commonly supposed to be involved as modulator in the release of the two nonapeptides vasopressin (AVP) and oxytocin into the blood stream. Previous studies showed that forced swimming fails to increase the release of AVP into the blood stream while its secretion into the hypothalamus is triggered. We investigated here whether hypothalamically acting NO contributes to the control of the AVP release into blood under forced swimming conditions. Intracerebral microdialysis and in situ hybridization were employed to analyze the activity of the nitrergic system within the supraoptic nucleus (SON), the hypothalamic origin of the HNS. A 10-min forced swimming session failed to significantly alter the local NO release as indicated both by nitrite and, the main by-product of NO synthesis, citrulline levels in microdialysis samples collected from the SON. Microdialysis administration of NO directly into the SON increased the concentration of AVP in plasma samples collected during simultaneous forced swimming. In an additional experiment the effect of the defined stressor exposure on the concentration of mRNA coding for nNOS within the SON was investigated by in situ hybridization. Forced swimming increased the expression of nNOS mRNA at two and four hours after onset of the stressor compared to untreated controls. Taken together, our results imply that NO within the SON does not contribute to the regulation of the secretory activity of HNS neurons during acute forced swimming. Increased nNOS mRNA in the SON after forced swimming and the increase in AVP release in the presence of exogenous NO under forced swimming points to a possible role of NO in the regulation of the HNS under repeated stressor exposure.

subject areas

  • Animals
  • Citrulline
  • Hypothalamo-Hypophyseal System
  • Male
  • Nitrergic Neurons
  • Nitric Oxide
  • Nitric Oxide Synthase
  • Oxytocin
  • Physical Conditioning, Animal
  • Physical Exertion
  • Rats
  • Rats, Wistar
  • Supraoptic Nucleus
  • Vasopressins
scroll to property group menus

Research

keywords

  • In situ hybridization
  • hypothalamonrurohypophyseal system
  • microdialysis
  • stress
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0939-4451

Digital Object Identifier (DOI)

  • 10.1007/s00726-003-0040-x

PubMed ID

  • 14752614
scroll to property group menus

Additional Document Info

start page

  • 37

end page

  • 43

volume

  • 26

issue

  • 1

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support