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10.1152/ajprenal.00463.2020 http://scihub22266oqcxt.onion/10.1152/ajprenal.00463.2020 33135481!7792700!33135481     free     free     free 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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2020 ; 319 (6): F1043-F1053 Nephropedia Template TP {{tp|p=33135481|t=2020. NaCl cotransporter activity and Mg(2+) handling by the distal convoluted tubule |pdf=|usr=}}{{33135481}} gab.com Text NaCl cotransporter activity and Mg(2+) handling by the distal convoluted tubule JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=33135481 #FOAvip The genetic disease Gitelman syndrome, knockout mice, and pharmacological blockade with thiazide diuretics have revealed that reduced activity of the NaCl cotransporter (NCC) promotes renal Mg(2+) wasting. NCC is expressed along the distal convoluted tubule (DCT), and its activity determines Mg(2+) entry into DCT cells through transient receptor potential channel subfamily M member 6 (TRPM6). Several other genetic forms of hypomagnesemia lower the drive for Mg(2+) entry by inhibiting activity of basolateral Na(+)-K(+)-ATPase, and reduced NCC activity may do the same. Lower intracellular Mg(2+) may promote further Mg(2+) loss by directly decreasing activity of Na(+)-K(+)-ATPase. Lower intracellular Mg(2+) may also lower Na(+)-K(+)-ATPase indirectly by downregulating NCC. Lower NCC activity also induces atrophy of DCT cells, decreasing the available number of TRPM6 channels. Conversely, a mouse model with increased NCC activity was recently shown to display normal Mg(2+) handling. Moreover, recent studies have identified calcineurin and uromodulin (UMOD) as regulators of both NCC and Mg(2+) handling by the DCT. Calcineurin inhibitors paradoxically cause hypomagnesemia in a state of NCC activation, but this may be related to direct effects on TRPM6 gene expression. In Umod(-/-) mice, the cause of hypomagnesemia may be partly due to both decreased NCC expression and lower TRPM6 expression on the cell surface. This mini-review discusses these new findings and the possible role of altered Na(+) flux through NCC and ultimately Na(+)-K(+)-ATPase in Mg(2+) reabsorption by the DCT. Twit Text FOAVip NaCl cotransporter activity and Mg(2+) handling by the distal convoluted tubule ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=33135481 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33135481 #FOAvip English Wikipedia <ref>{{Cite pmid|33135481}}</ref> NaCl cotransporter activity and Mg(2+) handling by the distal convoluted tubule #MMPMID33135481 Maeoka Y; McCormick JA Am J Physiol Renal Physiol 2020[Dec]; 319 (6): F1043-F1053 PMID33135481show ga The genetic disease Gitelman syndrome, knockout mice, and pharmacological blockade with thiazide diuretics have revealed that reduced activity of the NaCl cotransporter (NCC) promotes renal Mg(2+) wasting. NCC is expressed along the distal convoluted tubule (DCT), and its activity determines Mg(2+) entry into DCT cells through transient receptor potential channel subfamily M member 6 (TRPM6). Several other genetic forms of hypomagnesemia lower the drive for Mg(2+) entry by inhibiting activity of basolateral Na(+)-K(+)-ATPase, and reduced NCC activity may do the same. Lower intracellular Mg(2+) may promote further Mg(2+) loss by directly decreasing activity of Na(+)-K(+)-ATPase. Lower intracellular Mg(2+) may also lower Na(+)-K(+)-ATPase indirectly by downregulating NCC. Lower NCC activity also induces atrophy of DCT cells, decreasing the available number of TRPM6 channels. Conversely, a mouse model with increased NCC activity was recently shown to display normal Mg(2+) handling. Moreover, recent studies have identified calcineurin and uromodulin (UMOD) as regulators of both NCC and Mg(2+) handling by the DCT. Calcineurin inhibitors paradoxically cause hypomagnesemia in a state of NCC activation, but this may be related to direct effects on TRPM6 gene expression. In Umod(-/-) mice, the cause of hypomagnesemia may be partly due to both decreased NCC expression and lower TRPM6 expression on the cell surface. This mini-review discusses these new findings and the possible role of altered Na(+) flux through NCC and ultimately Na(+)-K(+)-ATPase in Mg(2+) reabsorption by the DCT. |*Renal Elimination[MESH] |*Renal Reabsorption[MESH] |Animals[MESH] |Calcineurin/metabolism[MESH] |Gitelman Syndrome/genetics/*metabolism/physiopathology[MESH] |Humans[MESH] |Kidney Tubules, Distal/*metabolism/physiopathology[MESH] |Magnesium/*metabolism[MESH] |Sodium-Potassium-Exchanging ATPase/metabolism[MESH] |Solute Carrier Family 12, Member 3/genetics/*metabolism[MESH] |TRPM Cation Channels/metabolism[MESH]NaCl cotransporter activity and Mg(2+) handling by the distal convolut(epmc).pdf DeepDyve Pubget Overpricing