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10.7150/ijbs.20074 http://scihub22266oqcxt.onion/10.7150/ijbs.20074 C5599902!5599902 !28924378     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28924378 &cmd=llinks): Failed to open stream: HTTP request failed! 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Vasopressin Mediates the Renal Damage Induced by Limited Fructose Rehydration in Recurrently Dehydrated Rats |pdf=|usr=}}{{28924378 }} gab.com Text Vasopressin Mediates the Renal Damage Induced by Limited Fructose Rehydration in Recurrently Dehydrated Rats JO: Int J Biol Sci http://www.kidney.de/pget.php?&tw=1&pmid=28924378 #FOAvip Recurrent dehydration and heat stress cause chronic kidney damage in experimental animals. The injury is exacerbated by rehydration with fructose-containing beverages. Fructose may amplify dehydration-induced injury by directly stimulating vasopressin release and also by acting as a substrate for the aldose reductase-fructokinase pathway, as both of these systems are active during dehydration. The role of vasopressin in heat stress associated injury has not to date been explored. Here we show that the amplification of renal damage mediated by fructose in thermal dehydration is mediated by vasopressin. Fructose rehydration markedly enhanced vasopressin (copeptin) levels and activation of the aldose reductase-fructokinase pathway in the kidney. Moreover, the amplification of the renal functional changes (decreased creatinine clearance and tubular injury with systemic inflammation, renal oxidative stress, and mitochondrial dysfunction) were prevented by the blockade of V1a and V2 vasopressin receptors with conivaptan. On the other hand, there are also other operative mechanisms when water is used as rehydration fluid that produce milder renal damage that is not fully corrected by vasopressin blockade. Therefore, we clearly showed evidence of the cross-talk between fructose, even at small doses, and vasopressin that interact to amplify the renal damage induced by dehydration. These data may be relevant for heat stress nephropathy as well as for other renal pathologies due to the current generalized consumption of fructose and deficient hydration habits. Twit Text FOAVip Vasopressin Mediates the Renal Damage Induced by Limited Fructose Rehydration in Recurrently Dehydrated Rats ????Int J Biol Sci http://www.kidney.de/pget.php?&tw=1&pmid=28924378 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28924378 #FOAvip English Wikipedia <ref>{{Cite pmid|28924378 }}</ref> Vasopressin Mediates the Renal Damage Induced by Limited Fructose Rehydration in Recurrently Dehydrated Rats #MMPMID28924378 García-Arroyo FE ; Tapia E ; Blas-Marron MG ; Gonzaga G ; Silverio O ; Cristóbal M ; Osorio H ; Arellano-Buendía AS ; Zazueta C ; Aparicio-Trejo OE ; Reyes-García JG ; Pedraza-Chaverri J ; Soto V ; Roncal-Jiménez C ; Johnson RJ ; Sánchez-Lozada LG Int J Biol Sci 2017[]; 13 (8 ): 961-975 PMID28924378 show ga Recurrent dehydration and heat stress cause chronic kidney damage in experimental animals. The injury is exacerbated by rehydration with fructose-containing beverages. Fructose may amplify dehydration-induced injury by directly stimulating vasopressin release and also by acting as a substrate for the aldose reductase-fructokinase pathway, as both of these systems are active during dehydration. The role of vasopressin in heat stress associated injury has not to date been explored. Here we show that the amplification of renal damage mediated by fructose in thermal dehydration is mediated by vasopressin. Fructose rehydration markedly enhanced vasopressin (copeptin) levels and activation of the aldose reductase-fructokinase pathway in the kidney. Moreover, the amplification of the renal functional changes (decreased creatinine clearance and tubular injury with systemic inflammation, renal oxidative stress, and mitochondrial dysfunction) were prevented by the blockade of V1a and V2 vasopressin receptors with conivaptan. On the other hand, there are also other operative mechanisms when water is used as rehydration fluid that produce milder renal damage that is not fully corrected by vasopressin blockade. Therefore, we clearly showed evidence of the cross-talk between fructose, even at small doses, and vasopressin that interact to amplify the renal damage induced by dehydration. These data may be relevant for heat stress nephropathy as well as for other renal pathologies due to the current generalized consumption of fructose and deficient hydration habits. |Animals [MESH] |Blood Pressure/physiology [MESH] |Body Weight [MESH] |Fructose/*metabolism [MESH] |Hemodynamics/physiology [MESH] |Immunohistochemistry [MESH] |Kidney/*metabolism/*pathology [MESH] |Male [MESH] |Oxidative Stress/physiology [MESH] |Rats [MESH] |Receptors, Vasopressin/metabolism [MESH] |Renal Insufficiency, Chronic/*metabolism [MESH]Vasopressin Mediates the Renal Damage Induced by Limited Fructose Rehy(epmc).pdf DeepDyve Pubget Overpricing