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10.1152/ajpheart.00023.2016 http://scihub22266oqcxt.onion/10.1152/ajpheart.00023.2016 C4935507!4935507 !27106038     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27106038 &cmd=llinks): Failed to open stream: HTTP request failed! 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Radiation-induced afferent arteriolar endothelial-dependent dysfunction involves decreased epoxygenase metabolites |pdf=|usr=}}{{27106038 }} gab.com Text Radiation-induced afferent arteriolar endothelial-dependent dysfunction involves decreased epoxygenase metabolites JO: Am J Physiol Heart Circ Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27106038 #FOAvip Chronic kidney disease is a known complication of hematopoietic stem cell transplant (HSCT) and can be caused by irradiation at the time of the HSCT. In our rat model there is a 6- to 8-wk latent period after irradiation that leads to the development of proteinuria, azotemia, and hypertension. The current study tested the hypothesis that decreased endothelial-derived factors contribute to impaired afferent arteriolar function in rats exposed to total body irradiation (TBI). WAG/RijCmcr rats underwent 11 Gy TBI, and afferent arteriolar responses to acetylcholine were determined at 1, 3, and 6 wk. Blood pressure and blood urea nitrogen were not different between control and irradiated rats. Afferent arteriolar diameters were not altered in irradiated rats. Impaired endothelial-dependent responses to acetylcholine were evident at 3 and 6 wk following TBI. Nitric oxide synthase (NOS), cyclooxygenase (COX), and epoxygenase (EPOX) contribution to acetylcholine dilator responses were evaluated. NOS inhibition with N(G)-nitro-l-arginine methyl ester (l-NAME) reduced acetylcholine responses by 50% in controls and 90% in 3-wk TBI rats. COX inhibition with indomethacin did not significantly alter the acetylcholine response in the presence or absence of l-NAME. EPOX inhibition with N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide significantly decreased acetylcholine responses (35%) in controls but did not significantly alter acetylcholine responses (4%) in TBI rats. Biochemical analysis revealed decreased urinary EPOX metabolites but no change in COX, NOS, or reactive oxygen species at 3 wk TBI. Taken together, these results indicate that afferent arteriolar endothelial dysfunction involves a decrease in EPOX metabolites that precedes the development of proteinuria, azotemia, and hypertension in irradiated rats. Twit Text FOAVip Radiation-induced afferent arteriolar endothelial-dependent dysfunction involves decreased epoxygenase metabolites ????Am J Physiol Heart Circ Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27106038 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27106038 #FOAvip English Wikipedia <ref>{{Cite pmid|27106038 }}</ref> Radiation-induced afferent arteriolar endothelial-dependent dysfunction involves decreased epoxygenase metabolites #MMPMID27106038 Imig JD ; Hye Khan MA ; Sharma A ; Fish BL ; Mandel NS ; Cohen EP Am J Physiol Heart Circ Physiol 2016[Jun]; 310 (11 ): H1695-701 PMID27106038 show ga Chronic kidney disease is a known complication of hematopoietic stem cell transplant (HSCT) and can be caused by irradiation at the time of the HSCT. In our rat model there is a 6- to 8-wk latent period after irradiation that leads to the development of proteinuria, azotemia, and hypertension. The current study tested the hypothesis that decreased endothelial-derived factors contribute to impaired afferent arteriolar function in rats exposed to total body irradiation (TBI). WAG/RijCmcr rats underwent 11 Gy TBI, and afferent arteriolar responses to acetylcholine were determined at 1, 3, and 6 wk. Blood pressure and blood urea nitrogen were not different between control and irradiated rats. Afferent arteriolar diameters were not altered in irradiated rats. Impaired endothelial-dependent responses to acetylcholine were evident at 3 and 6 wk following TBI. Nitric oxide synthase (NOS), cyclooxygenase (COX), and epoxygenase (EPOX) contribution to acetylcholine dilator responses were evaluated. NOS inhibition with N(G)-nitro-l-arginine methyl ester (l-NAME) reduced acetylcholine responses by 50% in controls and 90% in 3-wk TBI rats. COX inhibition with indomethacin did not significantly alter the acetylcholine response in the presence or absence of l-NAME. EPOX inhibition with N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide significantly decreased acetylcholine responses (35%) in controls but did not significantly alter acetylcholine responses (4%) in TBI rats. Biochemical analysis revealed decreased urinary EPOX metabolites but no change in COX, NOS, or reactive oxygen species at 3 wk TBI. Taken together, these results indicate that afferent arteriolar endothelial dysfunction involves a decrease in EPOX metabolites that precedes the development of proteinuria, azotemia, and hypertension in irradiated rats. |Acetylcholine/pharmacology [MESH] |Animals [MESH] |Arterioles/drug effects/metabolism/*radiation effects [MESH] |Blood Pressure/drug effects/*radiation effects [MESH] |Cyclooxygenase Inhibitors/pharmacology [MESH] |Endothelium, Vascular/drug effects/metabolism/*radiation effects [MESH] |Indomethacin/pharmacology [MESH] |Male [MESH] |NG-Nitroarginine Methyl Ester/pharmacology [MESH] |Nitric Oxide Synthase/antagonists & inhibitors/metabolism [MESH] |Prostaglandin-Endoperoxide Synthases/metabolism [MESH] |Rats [MESH] |Vasodilation/drug effects/*radiation effects [MESH]Radiation-induced afferent arteriolar endothelial-dependent dysfunctio(epmc).pdf DeepDyve Pubget Overpricing