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10.1161/01.RES.0000177669.29525.78 http://scihub22266oqcxt.onion/10.1161/01.RES.0000177669.29525.78 16020754!1352308!16020754     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Res 2005 ; 97 (4): 354-62 Nephropedia Template TP {{tp|p=16020754|t=2005. Mitochondria-derived reactive oxygen species dilate cerebral arteries by activating Ca2+ sparks |pdf=|usr=}}{{16020754}} gab.com Text Mitochondria-derived reactive oxygen species dilate cerebral arteries by activating Ca2+ sparks JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=16020754 #FOAvip Mitochondria regulate intracellular calcium (Ca2+) signals in smooth muscle cells, but mechanisms mediating these effects, and the functional relevance, are poorly understood. Similarly, antihypertensive ATP-sensitive potassium (KATP) channel openers (KCOs) activate plasma membrane KATP channels and depolarize mitochondria in several cell types, but the contribution of each of these mechanisms to vasodilation is unclear. Here, we show that cerebral artery smooth muscle cell mitochondria are most effectively depolarized by diazoxide (-15%, tetramethylrhodamine [TMRM]), less so by levcromakalim, and not depolarized by pinacidil. KCO-induced mitochondrial depolarization increased the generation of mitochondria-derived reactive oxygen species (ROS) that stimulated Ca2+ sparks and large-conductance Ca2+-activated potassium (KCa) channels, leading to transient KCa current activation. KCO-induced mitochondrial depolarization and transient KCa current activation were attenuated by 5-HD and glibenclamide, KATP channel blockers. MnTMPyP, an antioxidant, and Ca2+ spark and KCa channel blockers reduced diazoxide-induced vasodilations by >60%, but did not alter dilations induced by pinacidil, which did not elevate ROS. Data suggest diazoxide drives ROS generation by inducing a small mitochondrial depolarization, because nanomolar CCCP, a protonophore, similarly depolarized mitochondria, elevated ROS, and activated transient KCa currents. In contrast, micromolar CCCP, or rotenone, an electron transport chain blocker, induced a large mitochondrial depolarization (-84%, TMRM), reduced ROS, and inhibited transient KCa currents. In summary, data demonstrate that mitochondria-derived ROS dilate cerebral arteries by activating Ca2+ sparks, that some antihypertensive KCOs dilate by stimulating this pathway, and that small and large mitochondrial depolarizations lead to differential regulation of ROS and Ca2+ sparks. Twit Text FOAVip Mitochondria-derived reactive oxygen species dilate cerebral arteries by activating Ca2+ sparks ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=16020754 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=16020754 #FOAvip English Wikipedia <ref>{{Cite pmid|16020754}}</ref> Mitochondria-derived reactive oxygen species dilate cerebral arteries by activating Ca2+ sparks #MMPMID16020754 Xi Q; Cheranov SY; Jaggar JH Circ Res 2005[Aug]; 97 (4): 354-62 PMID16020754show ga Mitochondria regulate intracellular calcium (Ca2+) signals in smooth muscle cells, but mechanisms mediating these effects, and the functional relevance, are poorly understood. Similarly, antihypertensive ATP-sensitive potassium (KATP) channel openers (KCOs) activate plasma membrane KATP channels and depolarize mitochondria in several cell types, but the contribution of each of these mechanisms to vasodilation is unclear. Here, we show that cerebral artery smooth muscle cell mitochondria are most effectively depolarized by diazoxide (-15%, tetramethylrhodamine [TMRM]), less so by levcromakalim, and not depolarized by pinacidil. KCO-induced mitochondrial depolarization increased the generation of mitochondria-derived reactive oxygen species (ROS) that stimulated Ca2+ sparks and large-conductance Ca2+-activated potassium (KCa) channels, leading to transient KCa current activation. KCO-induced mitochondrial depolarization and transient KCa current activation were attenuated by 5-HD and glibenclamide, KATP channel blockers. MnTMPyP, an antioxidant, and Ca2+ spark and KCa channel blockers reduced diazoxide-induced vasodilations by >60%, but did not alter dilations induced by pinacidil, which did not elevate ROS. Data suggest diazoxide drives ROS generation by inducing a small mitochondrial depolarization, because nanomolar CCCP, a protonophore, similarly depolarized mitochondria, elevated ROS, and activated transient KCa currents. In contrast, micromolar CCCP, or rotenone, an electron transport chain blocker, induced a large mitochondrial depolarization (-84%, TMRM), reduced ROS, and inhibited transient KCa currents. In summary, data demonstrate that mitochondria-derived ROS dilate cerebral arteries by activating Ca2+ sparks, that some antihypertensive KCOs dilate by stimulating this pathway, and that small and large mitochondrial depolarizations lead to differential regulation of ROS and Ca2+ sparks. |*Reactive Oxygen Species[MESH] |*Vasodilation/drug effects[MESH] |Adenosine Triphosphate/pharmacology[MESH] |Animals[MESH] |Calcium/*metabolism[MESH] |Carbonyl Cyanide m-Chlorophenyl Hydrazone/analogs & derivatives/pharmacology[MESH] |Cerebral Arteries/*physiology[MESH] |Diazoxide/pharmacology[MESH] |Female[MESH] |Male[MESH] |Mitochondria/*physiology[MESH] |Muscle, Smooth, Vascular/physiology[MESH] |Potassium Channels/drug effects/*physiology[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH] |Rotenone/pharmacology[MESH] |Ryanodine Receptor Calcium Release Channel/physiology[MESH]Mitochondria-derived reactive oxygen species dilate cerebral arteries (epmc).pdf DeepDyve Pubget Overpricing