Cerebrovascular alterations in mice lacking neuronal nitric oxide synthase gene expression

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Atıf İçin Kopyala

Irikura K., Huang P. L., Ma J., Lee W. S., DALKARA T., Fishman M. C., ...Daha Fazla

Proceedings of the National Academy of Sciences of the United States of America, cilt.92, sa.15, ss.6823-6827, 1995 (Scopus)

• Yayın Türü: Makale / Tam Makale
• Cilt numarası: 92 Sayı: 15
• Basım Tarihi: 1995
• Doi Numarası: 10.1073/pnas.92.15.6823
• Dergi Adı: Proceedings of the National Academy of Sciences of the United States of America
• Derginin Tarandığı İndeksler: Scopus
• Sayfa Sayıları: ss.6823-6827
• Anahtar Kelimeler: acetylcholine, cerebral blood flow, hypercapnia, knockout mice, N(ω)-nitro-L-arginine
• Hacettepe Üniversitesi Adresli: Evet

Özet

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.