Nitric oxide limits pressor responses to sympathetic activation in rat spinal cord

Leonard F. Arnolda, Douglas J. McKitrick, Ida J. Llewellyn-Smith, Jane B. Minson

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

N-methyl D-aspartate (NMDA) receptor stimulation is known to activate nitric oxide (NO) synthase, an enzyme present in a high proportion of sympathetic preganglionic neurons. In this study, we have examined the possibility that NO modulates the pressor responses elicited by NMDA receptor stimulation in the spinal cord. In experiments on anesthetized rats, we determined whether intrathecal administration of either 3-morpholinylsydnoneimine chloride (SIN-1), an NO donor, or N(G)-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, affected the response to stimulation of spinal NMDA receptors by NMDA (1 pmol to 1 μmol in 10-μL intrathecal administration). Intrathecal NMDA resulted in dose-dependent increases in blood pressure. SIN-1 (100 nmol) attenuated the pressor responses to NMDA (F1,70 = 12, P=0.001). Conversely, L-NAME (1 nmol to 1 μmol) augmented the pressor response to NMDA in a dose-dependent manner (F3,161 = 28.3, P<0.001). The effect of L-NAME to amplify the pressor response to NMDA was reversed by L-arginine but not by D-arginine. These results indicate that endogenous synthesis of NO in the spinal cord limits the pressor response to stimulation of spinal NMDA receptors.

Original languageEnglish
Pages (from-to)1089-1092
Number of pages4
JournalHypertension
Volume36
Issue number6
DOIs
Publication statusPublished - Dec 2000
Externally publishedYes

Keywords

  • Blood pressure
  • L-NAME
  • Nitric oxide synthase
  • Sympathetic nervous system

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