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10.1038/ki.2008.145 http://scihub22266oqcxt.onion/10.1038/ki.2008.145 18418352!2562927!18418352     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18418352&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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\18418352.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Kidney+Int 2008 ; 74 (4): 418-26 Nephropedia Template TP {{tp|p=18418352|t=2008. Tubuloglomerular feedback: mechanistic insights from gene-manipulated mice |pdf=|usr=}}{{18418352}} gab.com Text Tubuloglomerular feedback: mechanistic insights from gene-manipulated mice JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=18418352 #FOAvip Tubuloglomerular feedback (TGF) describes a causal and direct relationship between tubular NaCl concentration at the end of the ascending limb of the loop of Henle and afferent arteriolar tone. The use of genetically altered mice has led to an expansion of our understanding of the mechanisms underlying the functional coupling of epithelial, mesangial, and vascular cells in TGF. Studies in mice with deletions of the A or B isoform of NKCC2 (Na,K,2Cl cotransporter) and of ROMK indicate that NaCl uptake is required for response initiation. A role for transcellular salt transport is suggested by the inhibitory effect of ouabain in mutant mice with an ouabain-sensitive alpha1 Na,K-ATPase. No effect on TGF was observed in NHE2- and H/K-ATPase-deficient mice. TGF responses are abolished in A1 adenosine receptor-deficient mice, and studies in mice with null mutations in NTPDase1 or ecto-5'-nucleotidase indicate that adenosine involved in TGF is mainly derived from dephosphorylation of released ATP. Angiotensin II is a required cofactor for the elicitation of TGF responses, as AT1 receptor or angiotensin-converting enzyme deficiencies reduce TGF responses, mostly by reducing adenosine effectiveness. Overall, the evidence from these studies in genetically altered mice indicates that transcellular NaCl transport induces the generation of adenosine that, in conjunction with angiotensin II, elicits afferent arteriolar constriction. Twit Text FOAVip Tubuloglomerular feedback: mechanistic insights from gene-manipulated mice ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=18418352 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18418352 #FOAvip English Wikipedia <ref>{{Cite pmid|18418352}}</ref> Tubuloglomerular feedback: mechanistic insights from gene-manipulated mice #MMPMID18418352 Schnermann J; Briggs JP Kidney Int 2008[Aug]; 74 (4): 418-26 PMID18418352show ga Tubuloglomerular feedback (TGF) describes a causal and direct relationship between tubular NaCl concentration at the end of the ascending limb of the loop of Henle and afferent arteriolar tone. The use of genetically altered mice has led to an expansion of our understanding of the mechanisms underlying the functional coupling of epithelial, mesangial, and vascular cells in TGF. Studies in mice with deletions of the A or B isoform of NKCC2 (Na,K,2Cl cotransporter) and of ROMK indicate that NaCl uptake is required for response initiation. A role for transcellular salt transport is suggested by the inhibitory effect of ouabain in mutant mice with an ouabain-sensitive alpha1 Na,K-ATPase. No effect on TGF was observed in NHE2- and H/K-ATPase-deficient mice. TGF responses are abolished in A1 adenosine receptor-deficient mice, and studies in mice with null mutations in NTPDase1 or ecto-5'-nucleotidase indicate that adenosine involved in TGF is mainly derived from dephosphorylation of released ATP. Angiotensin II is a required cofactor for the elicitation of TGF responses, as AT1 receptor or angiotensin-converting enzyme deficiencies reduce TGF responses, mostly by reducing adenosine effectiveness. Overall, the evidence from these studies in genetically altered mice indicates that transcellular NaCl transport induces the generation of adenosine that, in conjunction with angiotensin II, elicits afferent arteriolar constriction. |Adenosine Triphosphatases/metabolism[MESH] |Adenosine/metabolism[MESH] |Angiotensin II/metabolism[MESH] |Animals[MESH] |Feedback, Physiological/*physiology[MESH] |Kidney Glomerulus/blood supply/metabolism/*physiology[MESH] |Kidney Tubules/metabolism/*physiology[MESH] |Mice[MESH]Tubuloglomerular feedback: mechanistic insights from gene-manipulated (epmc).pdf DeepDyve Pubget Overpricing