• Media type: E-Article
  • Title: Cerebrovascular Alterations in Mice Lacking Neuronal Nitric Oxide Synthase Gene Expression
  • Contributor: Irikura, Katsumi; Huang, Paul L.; Ma, Jianya; Lee, Won Suk; Dalkara, Turgay; Fishman, Mark C.; Dawson, Ted M.; Snyder, Solomon H.; Moskowitz, Michael A.
  • Published: National Academy of Sciences of the United States of America, 1995
  • Published in: Proceedings of the National Academy of Sciences of the United States of America
  • Extent: 6823-6827
  • Language: English
  • ISSN: 0027-8424
  • Abstract: <p>Nitric oxide (NO) is known to mediate increases in regional cerebral blood flow elicited by CO<sub>2</sub>inhalation. In mice with deletion of the gene for neuronal NO synthase (NOS), CO<sub>2</sub>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<sup>ω</sup>-nitro-L-arginine, and CO<sub>2</sub>exposure fails to increase brain levels of cGMP. Topical acetylcholine elicits vasodilation in the mutants which is blocked by N<sup>ω</sup>-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.</p>
  • Description: <p>Nitric oxide (NO) is known to mediate increases in regional cerebral blood flow elicited by CO<sub>2</sub>inhalation. In mice with deletion of the gene for neuronal NO synthase (NOS), CO<sub>2</sub>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<sup>ω</sup>-nitro-L-arginine, and CO<sub>2</sub>exposure fails to increase brain levels of cGMP. Topical acetylcholine elicits vasodilation in the mutants which is blocked by N<sup>ω</sup>-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.</p>
  • Footnote:
  • Access State: Open Access