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10.1155/2015/535686 http://scihub22266oqcxt.onion/10.1155/2015/535686 C4396880!4396880 !25918583     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25918583 &cmd=llinks): Failed to open stream: HTTP request failed! 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Renal oxidative stress induced by long-term hyperuricemia alters mitochondrial function and maintains systemic hypertension |pdf=|usr=}}{{25918583 }} gab.com Text Renal oxidative stress induced by long-term hyperuricemia alters mitochondrial function and maintains systemic hypertension JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=25918583 #FOAvip We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia. A second objective was to evaluate whether the long-term treatment with the antioxidant Tempol prevents renal oxidative stress, mitochondrial alterations, and systemic hypertension in this model. Long-term (11-12 weeks) and short-term (3 weeks) effects of oxonic acid induced hyperuricemia were studied in rats (OA, 750?mg/kg BW), OA+Allopurinol (AP, 150?mg/L drinking water), OA+Tempol (T, 15?mg/kg BW), or vehicle. Systolic blood pressure, renal blood flow, and vascular resistance were measured. Tubular damage (urine N-acetyl-?-D-glucosaminidase) and oxidative stress markers (lipid and protein oxidation) along with ATP levels were determined in kidney tissue. Oxygen consumption, aconitase activity, and uric acid were evaluated in isolated mitochondria from renal cortex. Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction. Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels. Treatments with Tempol and allopurinol prevented these alterations. Renal oxidative stress induced by hyperuricemia promoted mitochondrial functional disturbances and decreased ATP content, which represent an additional pathogenic mechanism induced by chronic hyperuricemia. Hyperuricemia-related hypertension occurs before these changes are evident. Twit Text FOAVip Renal oxidative stress induced by long-term hyperuricemia alters mitochondrial function and maintains systemic hypertension ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=25918583 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25918583 #FOAvip English Wikipedia <ref>{{Cite pmid|25918583 }}</ref> Renal oxidative stress induced by long-term hyperuricemia alters mitochondrial function and maintains systemic hypertension #MMPMID25918583 Cristóbal-García M ; García-Arroyo FE ; Tapia E ; Osorio H ; Arellano-Buendía AS ; Madero M ; Rodríguez-Iturbe B ; Pedraza-Chaverrí J ; Correa F ; Zazueta C ; Johnson RJ ; Lozada LG Oxid Med Cell Longev 2015[]; 2015 (ä): 535686 PMID25918583 show ga We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia. A second objective was to evaluate whether the long-term treatment with the antioxidant Tempol prevents renal oxidative stress, mitochondrial alterations, and systemic hypertension in this model. Long-term (11-12 weeks) and short-term (3 weeks) effects of oxonic acid induced hyperuricemia were studied in rats (OA, 750?mg/kg BW), OA+Allopurinol (AP, 150?mg/L drinking water), OA+Tempol (T, 15?mg/kg BW), or vehicle. Systolic blood pressure, renal blood flow, and vascular resistance were measured. Tubular damage (urine N-acetyl-?-D-glucosaminidase) and oxidative stress markers (lipid and protein oxidation) along with ATP levels were determined in kidney tissue. Oxygen consumption, aconitase activity, and uric acid were evaluated in isolated mitochondria from renal cortex. Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction. Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels. Treatments with Tempol and allopurinol prevented these alterations. Renal oxidative stress induced by hyperuricemia promoted mitochondrial functional disturbances and decreased ATP content, which represent an additional pathogenic mechanism induced by chronic hyperuricemia. Hyperuricemia-related hypertension occurs before these changes are evident. |*Oxidative Stress/drug effects [MESH] |Adenosine Triphosphate/metabolism [MESH] |Allopurinol/pharmacology [MESH] |Animals [MESH] |Antioxidants/pharmacology [MESH] |Blood Pressure/drug effects [MESH] |Cyclic N-Oxides/pharmacology [MESH] |Disease Models, Animal [MESH] |Hypertension/etiology/*pathology [MESH] |Hyperuricemia/chemically induced/complications/*pathology [MESH] |Kidney/blood supply/*metabolism/pathology [MESH] |Male [MESH] |Mitochondria/drug effects/*metabolism [MESH] |Oxonic Acid/toxicity [MESH] |Oxygen Consumption [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Renal Circulation/drug effects [MESH] |Spin Labels [MESH]Renal oxidative stress induced by long-term hyperuricemia alters mitoc(epmc).pdf DeepDyve Pubget Overpricing