https://scholars.lib.ntu.edu.tw/handle/123456789/532767
標題: | Total sleep deprivation inhibits the neuronal nitric oxide synthase and cytochrome oxidase reactivities in the nodose ganglion of adult rats | 作者: | Chang H.-M. UN-IN WU Lin T.-B. Lan C.-T. Chien W.-C. Huang W.-L. Shieh J.-Y. |
公開日期: | 2006 | 卷: | 209 | 期: | 2 | 起(迄)頁: | 239-250 | 來源出版物: | Journal of Anatomy | 摘要: | Sleep disorders are a form of stress associated with increased sympathetic activity, and they are a risk factor for the occurrence of cardiovascular disease. Given that nitric oxide (NO) may play an inhibitory role in the regulation of sympathetic tone, this study set out to determine the NO synthase (NOS) reactivity in the primary cardiovascular afferent neurons (i.e. nodose neurons) following total sleep deprivation (TSD). TSD was performed by the disc-on-water method. Following 5.days of TSD, all experimental animals were investigated for quantitative nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d, a co-factor of NOS) histochemistry, neuronal NOS immunohistochemistry and neuronal NOS activity assay. In order to evaluate the endogenous metabolic activity of nodose neurons, cytochrome oxidase (COX) reactivity was further tested. All the above-mentioned reactivities were objectively assessed by computerized image analysis. The clinical significance of the reported changes was demonstrated by alterations of mean arterial blood pressure (MAP). The results indicated that in normal untreated rats, numerous NADPH-d/NOS- and COX-reactive neurons were found in the nodose ganglion (NG). Following TSD, however, both the labelling and staining intensity of NADPH-d/NOS as well as COX reactivity were drastically reduced in the NG compared with normal untreated ganglions. MAP was significantly higher in TSD rats (136 ± 4 mmHg) than in normal untreated rats (123 ± 2mmHg). NO may serve as an important sympathoinhibition messenger released by the NG neurons, and decrease of NOS immunoexpression following TSD may account for the decrease in NOS content. In association with the reduction of NOS activity, a defect in NOS expression in the primary cardiovascular afferent neurons would enhance clinical hypertension, which might serve as a potential risk factor in the development of TSD-relevant cardiovascular disturbances. ? 2006 The Authors Journal compilation ? 2006 Anatomical Society of Great Britain and Ireland. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-33746602616&doi=10.1111%2fj.1469-7580.2006.00594.x&partnerID=40&md5=f0be2b098b435d17a4fbebda01898e70 https://scholars.lib.ntu.edu.tw/handle/123456789/532767 |
ISSN: | 0021-8782 | DOI: | 10.1111/j.1469-7580.2006.00594.x | SDG/關鍵字: | cytochrome c oxidase; neuronal nitric oxide synthase; reduced nicotinamide adenine dinucleotide phosphate; animal cell; animal experiment; animal tissue; article; cell count; computer analysis; controlled study; enzyme activity; enzyme inhibition; histochemistry; image analysis; immunofluorescence; immunohistochemistry; immunoreactivity; male; mean arterial pressure; neuroimaging; nodose ganglion; nonhuman; priority journal; protein expression; quantitative analysis; rat; rat strain; sensory nerve; sleep deprivation; sympathetic tone; Animals; Blood Pressure; Cell Count; Electron Transport Complex IV; Hypertension; Male; NADPH Dehydrogenase; Nitric Oxide Synthase; Nodose Ganglion; Rats; Rats, Wistar; Sleep Deprivation; Animalia |
顯示於: | 醫學系 |
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