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10.1073/pnas.1604757113 http://scihub22266oqcxt.onion/10.1073/pnas.1604757113 C5024585!5024585 !27551068     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27551068 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Proc+Natl+Acad+Sci+U+S+A 2016 ; 113 (35 ): 9934-9 Nephropedia Template TP {{tp|p=27551068 |t=2016. Bioelectric impact of pathological angiogenesis on vascular function |pdf=|usr=}}{{27551068 }} gab.com Text Bioelectric impact of pathological angiogenesis on vascular function JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=27551068 #FOAvip Pathological angiogenesis, as seen in many inflammatory, immune, malignant, and ischemic disorders, remains an immense health burden despite new molecular therapies. It is likely that further therapeutic progress requires a better understanding of neovascular pathophysiology. Surprisingly, even though transmembrane voltage is well known to regulate vascular function, no previous bioelectric analysis of pathological angiogenesis has been reported. Using the perforated-patch technique to measure vascular voltages in human retinal neovascular specimens and rodent models of retinal neovascularization, we discovered that pathological neovessels generate extraordinarily high voltage. Electrophysiological experiments demonstrated that voltage from aberrantly located preretinal neovascular complexes is transmitted into the intraretinal vascular network. With extensive neovascularization, this voltage input is substantial and boosts the membrane potential of intraretinal blood vessels to a suprahyperpolarized level. Coincident with this suprahyperpolarization, the vasomotor response to hypoxia is fundamentally altered. Instead of the compensatory dilation observed in the normal retina, arterioles constrict in response to an oxygen deficiency. This anomalous vasoconstriction, which would potentiate hypoxia, raises the possibility that the bioelectric impact of neovascularization on vascular function is a previously unappreciated pathophysiological mechanism to sustain hypoxia-driven angiogenesis. Twit Text FOAVip Bioelectric impact of pathological angiogenesis on vascular function ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=27551068 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27551068 #FOAvip English Wikipedia <ref>{{Cite pmid|27551068 }}</ref> Bioelectric impact of pathological angiogenesis on vascular function #MMPMID27551068 Puro DG ; Kohmoto R ; Fujita Y ; Gardner TW ; Padovani-Claudio DA Proc Natl Acad Sci U S A 2016[Aug]; 113 (35 ): 9934-9 PMID27551068 show ga Pathological angiogenesis, as seen in many inflammatory, immune, malignant, and ischemic disorders, remains an immense health burden despite new molecular therapies. It is likely that further therapeutic progress requires a better understanding of neovascular pathophysiology. Surprisingly, even though transmembrane voltage is well known to regulate vascular function, no previous bioelectric analysis of pathological angiogenesis has been reported. Using the perforated-patch technique to measure vascular voltages in human retinal neovascular specimens and rodent models of retinal neovascularization, we discovered that pathological neovessels generate extraordinarily high voltage. Electrophysiological experiments demonstrated that voltage from aberrantly located preretinal neovascular complexes is transmitted into the intraretinal vascular network. With extensive neovascularization, this voltage input is substantial and boosts the membrane potential of intraretinal blood vessels to a suprahyperpolarized level. Coincident with this suprahyperpolarization, the vasomotor response to hypoxia is fundamentally altered. Instead of the compensatory dilation observed in the normal retina, arterioles constrict in response to an oxygen deficiency. This anomalous vasoconstriction, which would potentiate hypoxia, raises the possibility that the bioelectric impact of neovascularization on vascular function is a previously unappreciated pathophysiological mechanism to sustain hypoxia-driven angiogenesis. |*Electricity [MESH] |Animals [MESH] |Electrophysiology/instrumentation/methods [MESH] |Humans [MESH] |Hypoxia [MESH] |Membrane Potentials/physiology [MESH] |Mice, Inbred C57BL [MESH] |Microvessels/physiopathology [MESH] |Neovascularization, Pathologic/*physiopathology [MESH] |Rats, Long-Evans [MESH] |Retina/physiopathology [MESH] |Retinal Neovascularization/*physiopathology [MESH] |Retinal Vessels/*physiopathology [MESH]Bioelectric impact of pathological angiogenesis on vascular function (epmc).pdf DeepDyve Pubget Overpricing