Irikura, Katsumi;
Huang, Paul L.;
Ma, Jianya;
Lee, Won Suk;
Dalkara, Turgay;
Fishman, Mark C.;
Dawson, Ted M.;
Snyder, Solomon H.;
Moskowitz, Michael A.
Beteiligte:
Irikura, Katsumi;
Huang, Paul L.;
Ma, Jianya;
Lee, Won Suk;
Dalkara, Turgay;
Fishman, Mark C.;
Dawson, Ted M.;
Snyder, Solomon H.;
Moskowitz, Michael A.
Erschienen:
National Academy of Sciences of the United States of America, 1995
Erschienen in:Proceedings of the National Academy of Sciences of the United States of America
Umfang:
6823-6827
Sprache:
Englisch
ISSN:
0027-8424
Beschreibung:
<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>