{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:30:05Z","timestamp":1761561005705},"reference-count":50,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,10,24]],"date-time":"2005-10-24T00:00:00Z","timestamp":1130112000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2006,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hypoxia impairs neuromuscular transmission in the rat diaphragm. In previous studies, we have shown that nitric oxide (NO) plays a role in force modulation of the diaphragm under hypoxic conditions. The role of NO, a neurotransmitter, on neurotransmission in skeletal muscle under hypoxic conditions is unknown. The effects of the NO synthase (NOS) inhibitor nomega\u2010nitro\u2010<jats:sc>L<\/jats:sc>\u2010arginine (<jats:sc>L<\/jats:sc>\u2010NNA, 1 mM) and the NO donor spermine NONOate (Sp\u2010NO, 1 mM) were evaluated on neurotransmission failure during nonfatiguing and fatiguing contractions of the rat diaphragm under hypoxic (P<jats:sc>O<\/jats:sc><jats:sub>2<\/jats:sub> \u223c 5.8 kPa) and hyperoxic conditions (P<jats:sc>O<\/jats:sc><jats:sub>2<\/jats:sub> \u223c 64.0 kPa). Hypoxia impaired force generated by both muscle stimulation at 40 H<jats:sc>Z<\/jats:sc> (P<jats:sub>40<\/jats:sub>M) and by nerve stimulation at 40 H<jats:sc>Z<\/jats:sc> (P<jats:sub>40<\/jats:sub>N). The effect of hypoxia in the latter was more pronounced. <jats:sc>L<\/jats:sc>\u2010NNA increased P<jats:sub>40<\/jats:sub>N whereas Sp\u2010NO decreased P<jats:sub>40<\/jats:sub>N during hypoxia. In contrast, neither <jats:sc>L<\/jats:sc>\u2010NNA nor Sp\u2010NO affected P<jats:sub>40<\/jats:sub>N during hyperoxia. <jats:sc>L<\/jats:sc>\u2010NNA only slightly reduced neurotransmission failure during fatiguing contractions under hyperoxic conditions. Consequently, neurotransmission failure assessed by comparing force loss during repetitive nerve simulation and superimposed direct muscle stimulation was more pronounced in hypoxia, which was alleviated by <jats:sc>L<\/jats:sc>\u2010NNA and aggravated by Sp\u2010NO. These data provide insight in the underlying mechanisms of hypoxia\u2010induced neurotransmission failure. This is important as respiratory muscle failure may result from hypoxia in vivo. 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