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10.1016/j.redox.2018.02.006 http://scihub22266oqcxt.onion/10.1016/j.redox.2018.02.006 C5854893!5854893 !29524844     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29524844 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Redox+Biol 2018 ; 16 (ä): 215-225 Nephropedia Template TP {{tp|p=29524844 |t=2018. Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascular relaxation: Role of insufficient hydrogen sulfide |pdf=|usr=}}{{29524844 }} gab.com Text Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascular relaxation: Role of insufficient hydrogen sulfide JO: Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=29524844 #FOAvip Insufficient hydrogen sulfide (H(2)S) has been implicated in Type 2 diabetic mellitus (T2DM) and hyperhomocysteinemia (HHcy)-related cardiovascular complications. We investigated the role of H(2)S in T2DM and HHcy-induced endothelial dysfunction in small mesenteric artery (SMA) of db/db mice fed a high methionine (HM) diet. HM diet (8 weeks) induced HHcy in both T2DM db/db mice and non-diabetic db/+ mice (total plasma Hcy: 48.4 and 31.3?µM, respectively), and aggravated the impaired endothelium-derived hyperpolarization factor (EDHF)-induced endothelium-dependent relaxation to acetylcholine (ACh), determined by the presence of eNOS inhibitor N(?)-nitro-L-arginine methyl ester (L-NAME) and prostacyclin (PGI(2)) inhibitor indomethacin (INDO), in SMA from db/db mice but not that from db/+ mice. A non-selective Ca(2+)-active potassium channel (K(Ca)) opener NS309 rescued T2DM/HHcy-impaired EDHF-mediated vascular relaxation to ACh. EDHF-induced relaxation to ACh was inhibited by a non-selective K(Ca) blocker TEA and intermediate-conductance K(Ca) blocker (IK(Ca)) Tram-34, but not by small-conductance K(Ca) (SK(Ca)) blocker Apamin. HHcy potentiated the reduction of free sulfide, H(2)S and cystathionine ?-lyase protein, which converts L-cysteine to H(2)S, in SMA of db/db mice. Importantly, a stable H(2)S donor DATS diminished the enhanced O(2)(-) production in SMAs and lung endothelial cells of T2DM/HHcy mice. Antioxidant PEG-SOD and DATS improved T2DM/HHcy impaired relaxation to ACh. Moreover, HHcy increased hyperglycemia-induced IK(Ca) tyrosine nitration in human micro-vascular endothelial cells. EDHF-induced vascular relaxation to L-cysteine was not altered, whereas such relaxation to NaHS was potentiated by HHcy in SMA of db/db mice which was abolished by ATP-sensitive potassium channel blocker Glycolamide but not by K(Ca) blockers. CONCLUSIONS: Intermediate HHcy potentiated H(2)S reduction via CSE-downregulation in microvasculature of T2DM mice. H(2)S is justified as an EDHF. Insufficient H(2)S impaired EDHF-induced vascular relaxation via oxidative stress and IK(Ca) inactivation in T2DM/HHcy mice. H(2)S therapy may be beneficial for prevention and treatment of micro-vascular complications in patients with T2DM and HHcy. Twit Text FOAVip Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascular relaxation: Role of insufficient hydrogen sulfide ????Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=29524844 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29524844 #FOAvip English Wikipedia <ref>{{Cite pmid|29524844 }}</ref> Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascular relaxation: Role of insufficient hydrogen sulfide #MMPMID29524844 Cheng Z ; Shen X ; Jiang X ; Shan H ; Cimini M ; Fang P ; Ji Y ; Park JY ; Drosatos K ; Yang X ; Kevil CG ; Kishore R ; Wang H Redox Biol 2018[Jun]; 16 (ä): 215-225 PMID29524844 show ga Insufficient hydrogen sulfide (H(2)S) has been implicated in Type 2 diabetic mellitus (T2DM) and hyperhomocysteinemia (HHcy)-related cardiovascular complications. We investigated the role of H(2)S in T2DM and HHcy-induced endothelial dysfunction in small mesenteric artery (SMA) of db/db mice fed a high methionine (HM) diet. HM diet (8 weeks) induced HHcy in both T2DM db/db mice and non-diabetic db/+ mice (total plasma Hcy: 48.4 and 31.3?µM, respectively), and aggravated the impaired endothelium-derived hyperpolarization factor (EDHF)-induced endothelium-dependent relaxation to acetylcholine (ACh), determined by the presence of eNOS inhibitor N(?)-nitro-L-arginine methyl ester (L-NAME) and prostacyclin (PGI(2)) inhibitor indomethacin (INDO), in SMA from db/db mice but not that from db/+ mice. A non-selective Ca(2+)-active potassium channel (K(Ca)) opener NS309 rescued T2DM/HHcy-impaired EDHF-mediated vascular relaxation to ACh. EDHF-induced relaxation to ACh was inhibited by a non-selective K(Ca) blocker TEA and intermediate-conductance K(Ca) blocker (IK(Ca)) Tram-34, but not by small-conductance K(Ca) (SK(Ca)) blocker Apamin. HHcy potentiated the reduction of free sulfide, H(2)S and cystathionine ?-lyase protein, which converts L-cysteine to H(2)S, in SMA of db/db mice. Importantly, a stable H(2)S donor DATS diminished the enhanced O(2)(-) production in SMAs and lung endothelial cells of T2DM/HHcy mice. Antioxidant PEG-SOD and DATS improved T2DM/HHcy impaired relaxation to ACh. Moreover, HHcy increased hyperglycemia-induced IK(Ca) tyrosine nitration in human micro-vascular endothelial cells. EDHF-induced vascular relaxation to L-cysteine was not altered, whereas such relaxation to NaHS was potentiated by HHcy in SMA of db/db mice which was abolished by ATP-sensitive potassium channel blocker Glycolamide but not by K(Ca) blockers. CONCLUSIONS: Intermediate HHcy potentiated H(2)S reduction via CSE-downregulation in microvasculature of T2DM mice. H(2)S is justified as an EDHF. Insufficient H(2)S impaired EDHF-induced vascular relaxation via oxidative stress and IK(Ca) inactivation in T2DM/HHcy mice. H(2)S therapy may be beneficial for prevention and treatment of micro-vascular complications in patients with T2DM and HHcy. |Acetylcholine/metabolism [MESH] |Animals [MESH] |Biological Factors/*metabolism [MESH] |Cardiovascular Diseases/genetics/metabolism/pathology [MESH] |Diabetes Mellitus, Type 2/genetics/*metabolism/pathology [MESH] |Endothelium, Vascular/metabolism/pathology [MESH] |Humans [MESH] |Hydrogen Sulfide/*metabolism [MESH] |Hyperhomocysteinemia/genetics/*metabolism/pathology [MESH] |Mesenteric Arteries/metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred NOD [MESH] |Nitric Oxide/metabolism [MESH] |Potassium Channel Blockers/metabolism [MESH]Hyperhomocysteinemia potentiates diabetes-impaired EDHF-induced vascul(epmc).pdf DeepDyve Pubget Overpricing