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10.1126/scisignal.aaf3204 http://scihub22266oqcxt.onion/10.1126/scisignal.aaf3204 C5505181!5505181 !27531649     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27531649 &cmd=llinks): Failed to open stream: HTTP request failed! 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H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea |pdf=|usr=}}{{27531649 }} gab.com Text H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea JO: Sci Signal http://www.kidney.de/pget.php?&tw=1&pmid=27531649 #FOAvip Sleep apnea is a prevalent respiratory disease in which episodic cessation of breathing causes intermittent hypoxia. Patients with sleep apnea and rodents exposed to intermittent hypoxia exhibit hypertension. The carotid body senses changes in blood O2 concentrations, and an enhanced carotid body chemosensory reflex contributes to hypertension in sleep apnea patients. A rodent model of intermittent hypoxia that mimics blood O2 saturation profiles of patients with sleep apnea has shown that increased generation of reactive oxygen species (ROS) in the carotid body enhances the chemosensory reflex and triggers hypertension. CO generated by heme oxygenase-2 (HO-2) induces a signaling pathway that inhibits hydrogen sulfide (H2S) production by cystathionine ?-lyase (CSE), leading to suppression of carotid body activity. We found that ROS inhibited CO generation by HO-2 in the carotid body and liver through a mechanism that required Cys(265) in the heme regulatory motif of heterologously expressed HO-2. We showed that ROS induced by intermittent hypoxia inhibited CO production and increased H2S concentrations in the carotid body, which stimulated its neural activity. In rodents, blockade of H2S synthesis by CSE, by either pharmacologic or genetic approaches, inhibited carotid body activation and hypertension induced by intermittent hypoxia. Thus, our results indicate that oxidant-induced inactivation of HO-2, which leads to increased CSE-dependent H2S production in the carotid body, is a critical trigger of hypertension in rodents exposed to intermittent hypoxia. Twit Text FOAVip H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea ????Sci Signal http://www.kidney.de/pget.php?&tw=1&pmid=27531649 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27531649 #FOAvip English Wikipedia <ref>{{Cite pmid|27531649 }}</ref> H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea #MMPMID27531649 Yuan G ; Peng YJ ; Khan SA ; Nanduri J ; Singh A ; Vasavda C ; Semenza GL ; Kumar GK ; Snyder SH ; Prabhakar NR Sci Signal 2016[Aug]; 9 (441 ): ra80 PMID27531649 show ga Sleep apnea is a prevalent respiratory disease in which episodic cessation of breathing causes intermittent hypoxia. Patients with sleep apnea and rodents exposed to intermittent hypoxia exhibit hypertension. The carotid body senses changes in blood O2 concentrations, and an enhanced carotid body chemosensory reflex contributes to hypertension in sleep apnea patients. A rodent model of intermittent hypoxia that mimics blood O2 saturation profiles of patients with sleep apnea has shown that increased generation of reactive oxygen species (ROS) in the carotid body enhances the chemosensory reflex and triggers hypertension. CO generated by heme oxygenase-2 (HO-2) induces a signaling pathway that inhibits hydrogen sulfide (H2S) production by cystathionine ?-lyase (CSE), leading to suppression of carotid body activity. We found that ROS inhibited CO generation by HO-2 in the carotid body and liver through a mechanism that required Cys(265) in the heme regulatory motif of heterologously expressed HO-2. We showed that ROS induced by intermittent hypoxia inhibited CO production and increased H2S concentrations in the carotid body, which stimulated its neural activity. In rodents, blockade of H2S synthesis by CSE, by either pharmacologic or genetic approaches, inhibited carotid body activation and hypertension induced by intermittent hypoxia. Thus, our results indicate that oxidant-induced inactivation of HO-2, which leads to increased CSE-dependent H2S production in the carotid body, is a critical trigger of hypertension in rodents exposed to intermittent hypoxia. |Animals [MESH] |Carotid Body/*metabolism/physiopathology [MESH] |Cystathionine gamma-Lyase/genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Heme Oxygenase (Decyclizing)/genetics/metabolism [MESH] |Hydrogen Sulfide/*metabolism [MESH] |Hypertension/genetics/*metabolism/physiopathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Reactive Oxygen Species/*metabolism [MESH]H2S production by reactive oxygen species in the carotid body triggers(epmc).pdf DeepDyve Pubget Overpricing