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10.14814/phy2.13728 http://scihub22266oqcxt.onion/10.14814/phy2.13728 30030908!6054696!30030908     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Physiol+Rep 2018 ; 6 (14): e13728 Nephropedia Template TP {{tp|p=30030908|t=2018. Renal sodium and magnesium reabsorption are not coupled in a mouse model of Gordon syndrome |pdf=|usr=}}{{30030908}} gab.com Text Renal sodium and magnesium reabsorption are not coupled in a mouse model of Gordon syndrome JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=30030908 #FOAvip Active reabsorption of magnesium (Mg(2+) ) in the distal convoluted tubule (DCT) of the kidney is crucial for maintaining Mg(2+) homeostasis. Impaired activity of the Na(+) -Cl(-) -cotransporter (NCC) has been associated with hypermagnesiuria and hypomagnesemia, while increased activity of NCC, as observed in patients with Gordon syndrome, is not associated with alterations in Mg(2+) balance. To further elucidate the possible interrelationship between NCC activity and renal Mg(2+) handling, plasma Mg(2+) levels and urinary excretion of sodium (Na(+) ) and Mg(2+) were measured in a mouse model of Gordon syndrome. In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na(+) reabsorption. These mice were normomagnesemic and HCTZ administration comparably reduced plasma Mg(2+) levels in CA-SPAK mice and control littermates. As inferred by the initial response to HCTZ, CA-SPAK mice exhibited greater NCC-dependent Na(+) reabsorption together with decreased Mg(2+) reabsorption, compared to controls. Following prolonged HCTZ administration (4 days), CA-SPAK mice exhibited higher urinary Mg(2+) excretion, while urinary Na(+) excretion decreased to levels observed in control animals. Surprisingly, CA-SPAK mice had unaltered renal expression of Trpm6, encoding the Mg(2+) -permeable channel TRPM6, or other magnesiotropic genes. In conclusion, CA-SPAK mice exhibit normomagnesemia, despite increased NCC activity and Na(+) reabsorption. Thus, Mg(2+) reabsorption is not coupled to increased thiazide-sensitive Na(+) reabsorption, suggesting a similar process explains normomagnesemia in Gordon syndrome. Further research is required to unravel the molecular underpinnings of this phenomenon and the more pronounced Mg(2+) excretion after prolonged HCTZ administration. Twit Text FOAVip Renal sodium and magnesium reabsorption are not coupled in a mouse model of Gordon syndrome ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=30030908 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30030908 #FOAvip English Wikipedia <ref>{{Cite pmid|30030908}}</ref> Renal sodium and magnesium reabsorption are not coupled in a mouse model of Gordon syndrome #MMPMID30030908 van Megen WH; Grimm PR; Welling PA; van der Wijst J Physiol Rep 2018[Jul]; 6 (14): e13728 PMID30030908show ga Active reabsorption of magnesium (Mg(2+) ) in the distal convoluted tubule (DCT) of the kidney is crucial for maintaining Mg(2+) homeostasis. Impaired activity of the Na(+) -Cl(-) -cotransporter (NCC) has been associated with hypermagnesiuria and hypomagnesemia, while increased activity of NCC, as observed in patients with Gordon syndrome, is not associated with alterations in Mg(2+) balance. To further elucidate the possible interrelationship between NCC activity and renal Mg(2+) handling, plasma Mg(2+) levels and urinary excretion of sodium (Na(+) ) and Mg(2+) were measured in a mouse model of Gordon syndrome. In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na(+) reabsorption. These mice were normomagnesemic and HCTZ administration comparably reduced plasma Mg(2+) levels in CA-SPAK mice and control littermates. As inferred by the initial response to HCTZ, CA-SPAK mice exhibited greater NCC-dependent Na(+) reabsorption together with decreased Mg(2+) reabsorption, compared to controls. Following prolonged HCTZ administration (4 days), CA-SPAK mice exhibited higher urinary Mg(2+) excretion, while urinary Na(+) excretion decreased to levels observed in control animals. Surprisingly, CA-SPAK mice had unaltered renal expression of Trpm6, encoding the Mg(2+) -permeable channel TRPM6, or other magnesiotropic genes. In conclusion, CA-SPAK mice exhibit normomagnesemia, despite increased NCC activity and Na(+) reabsorption. Thus, Mg(2+) reabsorption is not coupled to increased thiazide-sensitive Na(+) reabsorption, suggesting a similar process explains normomagnesemia in Gordon syndrome. Further research is required to unravel the molecular underpinnings of this phenomenon and the more pronounced Mg(2+) excretion after prolonged HCTZ administration. |*Renal Reabsorption[MESH] |Animals[MESH] |Arthrogryposis/*metabolism[MESH] |Cation Transport Proteins/genetics/metabolism[MESH] |Cleft Palate/*metabolism[MESH] |Clubfoot/*metabolism[MESH] |Female[MESH] |Hand Deformities, Congenital/*metabolism[MESH] |Hydrochlorothiazide/pharmacology[MESH] |Kidney/drug effects/metabolism[MESH] |Magnesium/*metabolism[MESH] |Male[MESH] |Mice[MESH] |Protein Serine-Threonine Kinases/genetics/metabolism[MESH] |Sodium Chloride Symporter Inhibitors/pharmacology[MESH] |Sodium/*metabolism[MESH] |Solute Carrier Family 12, Member 3/genetics/metabolism[MESH]Renal sodium and magnesium reabsorption are not coupled in a mouse mod(epmc).pdf DeepDyve Pubget Overpricing