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10.1016/j.bbrep.2017.09.010 http://scihub22266oqcxt.onion/10.1016/j.bbrep.2017.09.010 C5683885!5683885 !29159314     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29159314 &cmd=llinks): Failed to open stream: HTTP request failed! 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Vasoconstriction triggered by hydrogen sulfide: Evidence for Na(+),K(+),2Cl(-)cotransport and L-type Ca(2+) channel-mediated pathway |pdf=|usr=}}{{29159314 }} gab.com Text Vasoconstriction triggered by hydrogen sulfide: Evidence for Na(+),K(+),2Cl(-)cotransport and L-type Ca(2+) channel-mediated pathway JO: Biochem Biophys Rep http://www.kidney.de/pget.php?&tw=1&pmid=29159314 #FOAvip OBJECTIVES: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC). METHODS: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na(+)/K(+)-pump and Na(+),K(+),2Cl(-)cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the (86)Rb influx, respectively. RESULTS: NaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K(+)](o)=30 mM). At 10(-4) M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10(-3) M it decreased contractile responses by more than two-fold. Contractions evoked by 10(-4) M NaHS were completely abolished by bumetanide, a potent inhibitor of Na(+),K(+),2Cl(-)cotransport, whereas the inhibition seen at 10(-3) M NaHS was suppressed in the presence of K(+) channel blocker TEA. In cultured SMC, 5×10(-5) M NaHS increased Na(+),K(+),2Cl(-) - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, (45)Ca influx was enhanced in the presence of 10(-4) M NaHS and suppressed under elevation of [NaHS] up to 10(-3) M. (45)Ca influx triggered by 10(-4) M NaHS was abolished by bumetanide and L-type Ca(2+) channel blocker nicardipine. CONCLUSIONS: Our results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na(+),K(+),2Cl(-)cotransport and Ca(2+) influx via L-type channels. Twit Text FOAVip Vasoconstriction triggered by hydrogen sulfide: Evidence for Na(+),K(+),2Cl(-)cotransport and L-type Ca(2+) channel-mediated pathway ????Biochem Biophys Rep http://www.kidney.de/pget.php?&tw=1&pmid=29159314 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29159314 #FOAvip English Wikipedia <ref>{{Cite pmid|29159314 }}</ref> Vasoconstriction triggered by hydrogen sulfide: Evidence for Na(+),K(+),2Cl(-)cotransport and L-type Ca(2+) channel-mediated pathway #MMPMID29159314 Orlov SN ; Gusakova SV ; Smaglii LV ; Koltsova SV ; Sidorenko SV Biochem Biophys Rep 2017[Dec]; 12 (ä): 220-227 PMID29159314 show ga OBJECTIVES: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC). METHODS: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na(+)/K(+)-pump and Na(+),K(+),2Cl(-)cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the (86)Rb influx, respectively. RESULTS: NaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K(+)](o)=30 mM). At 10(-4) M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10(-3) M it decreased contractile responses by more than two-fold. Contractions evoked by 10(-4) M NaHS were completely abolished by bumetanide, a potent inhibitor of Na(+),K(+),2Cl(-)cotransport, whereas the inhibition seen at 10(-3) M NaHS was suppressed in the presence of K(+) channel blocker TEA. In cultured SMC, 5×10(-5) M NaHS increased Na(+),K(+),2Cl(-) - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, (45)Ca influx was enhanced in the presence of 10(-4) M NaHS and suppressed under elevation of [NaHS] up to 10(-3) M. (45)Ca influx triggered by 10(-4) M NaHS was abolished by bumetanide and L-type Ca(2+) channel blocker nicardipine. CONCLUSIONS: Our results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na(+),K(+),2Cl(-)cotransport and Ca(2+) influx via L-type channels. äVasoconstriction triggered by hydrogen sulfide: Evidence for Na(+),K(epmc).pdf DeepDyve Pubget Overpricing