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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. Using a rodent model of intermittent hypoxia that simulates blood O2-saturation profiles of patients with sleep apnea, increased generation of reactive oxygen species (ROS) in the carotid body has been shown to enhance the chemosensory reflex and trigger hypertension. Here, we report that ROS inhibited CO generation by heme oxygenase-2 (HO-2), a process that requires Cys265 in the heme regulatory motif of HO-2. CO binds to guanylate cyclase to increase production of cGMP, which stimulates protein kinase G-dependent phosphorylation and inactivation of the H2S-producing enzyme cystathionine-?-lyase (CSE). We showed that ROS induced by intermittent hypoxia inhibited CO production and increased H2S concentrations, which stimulated carotid body neural activity. Blockade of H2S synthesis by CSE either by pharmacological or genetic approaches inhibited carotid body activation and hypertension induced by intermittent hypoxia. Thus, oxidant-induced inactivation of HO-2 leading 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 PMID27531649show 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. Using a rodent model of intermittent hypoxia that simulates blood O2-saturation profiles of patients with sleep apnea, increased generation of reactive oxygen species (ROS) in the carotid body has been shown to enhance the chemosensory reflex and trigger hypertension. Here, we report that ROS inhibited CO generation by heme oxygenase-2 (HO-2), a process that requires Cys265 in the heme regulatory motif of HO-2. CO binds to guanylate cyclase to increase production of cGMP, which stimulates protein kinase G-dependent phosphorylation and inactivation of the H2S-producing enzyme cystathionine-?-lyase (CSE). We showed that ROS induced by intermittent hypoxia inhibited CO production and increased H2S concentrations, which stimulated carotid body neural activity. Blockade of H2S synthesis by CSE either by pharmacological or genetic approaches inhibited carotid body activation and hypertension induced by intermittent hypoxia. Thus, oxidant-induced inactivation of HO-2 leading to increased CSE-dependent H2S production in the carotid body is a critical trigger of hypertension in rodents exposed to intermittent hypoxia. äH2S Production by Reactive Oxygen Species in the Carotid Body Triggers(epmc).pdf DeepDyve Pubget Overpricing