Cerebrovascular alterations in mice lacking neuronal nitric oxide synthase gene expression

Katsumi Irikura, Paul L. Huang, Jianya Ma, Won Suk Lee, Turgay Dalkara, Mark C. Fishman, Ted M. Dawson, Solomon H. Snyder, Michael A. Moskowitz

Research output: Contribution to journalArticlepeer-review

Abstract

Nitric oxide (NO) is known to mediate increases in regional cerebral blood flow elicited by CO2 inhalation. In mice with deletion of the gene for neuronal NO synthase (NOS), CO2 inhalation augments cerebral blood flow to the same extent as in wild-type mice. However, unlike wild-type mice, the increased flow in mutants is not blocked by the NOS inhibition, N(ω)-nitro- L-arginine, and CO2 exposure fails to increase brain levels of cGMP. Topical acetylcholine elicits vasodilation in the mutants which is blocked by N(ω)- nitro-L-arginine, indicating normal functioning of endothelial NOS. Moreover, immunohistochemical staining for endothelial NOS is normal in the mutants. Thus, following loss of neuronal NOS, the cerebral circulatory response is maintained by a compensatory system not involving NO.

Original languageEnglish (US)
Pages (from-to)6823-6827
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume92
Issue number15
DOIs
StatePublished - Jul 18 1995

Keywords

  • N(ω)-nitro-L-arginine
  • acetylcholine
  • cerebral blood flow
  • hypercapnia
  • knockout mice

ASJC Scopus subject areas

  • General

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