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10.1016/j.kint.2016.10.038 http://scihub22266oqcxt.onion/10.1016/j.kint.2016.10.038 28094030!6034684!28094030     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 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 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       Kidney+Int 2017 ; 91 (5): 1159-1177 Nephropedia Template TP {{tp|p=28094030|t=2017. Glucocorticoid-induced leucine zipper protein regulates sodium and potassium balance in the distal nephron |pdf=|usr=}}{{28094030}} gab.com Text Glucocorticoid-induced leucine zipper protein regulates sodium and potassium balance in the distal nephron JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=28094030 #FOAvip Glucocorticoid induced leucine zipper protein (GILZ) is an aldosterone-regulated protein that controls sodium transport in cultured kidney epithelial cells. Mice lacking GILZ have been reported previously to have electrolyte abnormalities. However, the mechanistic basis has not been explored. Here we provide evidence supporting a role for GILZ in modulating the balance of renal sodium and potassium excretion by regulating the sodium-chloride cotransporter (NCC) activity in the distal nephron. Gilz(-/-) mice have a higher plasma potassium concentration and lower fractional excretion of potassium than wild type mice. Furthermore, knockout mice are more sensitive to NCC inhibition by thiazides than are the wild type mice, and their phosphorylated NCC expression is higher. Despite increased NCC activity, knockout mice do not have higher blood pressure than wild type mice. However, during sodium deprivation, knockout mice come into sodium balance more quickly, than do the wild type, without a significant increase in plasma renin activity. Upon prolonged sodium restriction, knockout mice develop frank hyperkalemia. Finally, in HEK293T cells, exogenous GILZ inhibits NCC activity at least in part by inhibiting SPAK phosphorylation. Thus, GILZ promotes potassium secretion by inhibiting NCC and enhancing distal sodium delivery to the epithelial sodium channel. Additionally, Gilz(-/-) mice have features resembling familial hyperkalemic hypertension, a human disorder that manifests with hyperkalemia associated variably with hypertension. Twit Text FOAVip Glucocorticoid-induced leucine zipper protein regulates sodium and potassium balance in the distal nephron ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=28094030 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28094030 #FOAvip English Wikipedia <ref>{{Cite pmid|28094030}}</ref> Glucocorticoid-induced leucine zipper protein regulates sodium and potassium balance in the distal nephron #MMPMID28094030 Rashmi P; Colussi G; Ng M; Wu X; Kidwai A; Pearce D Kidney Int 2017[May]; 91 (5): 1159-1177 PMID28094030show ga Glucocorticoid induced leucine zipper protein (GILZ) is an aldosterone-regulated protein that controls sodium transport in cultured kidney epithelial cells. Mice lacking GILZ have been reported previously to have electrolyte abnormalities. However, the mechanistic basis has not been explored. Here we provide evidence supporting a role for GILZ in modulating the balance of renal sodium and potassium excretion by regulating the sodium-chloride cotransporter (NCC) activity in the distal nephron. Gilz(-/-) mice have a higher plasma potassium concentration and lower fractional excretion of potassium than wild type mice. Furthermore, knockout mice are more sensitive to NCC inhibition by thiazides than are the wild type mice, and their phosphorylated NCC expression is higher. Despite increased NCC activity, knockout mice do not have higher blood pressure than wild type mice. However, during sodium deprivation, knockout mice come into sodium balance more quickly, than do the wild type, without a significant increase in plasma renin activity. Upon prolonged sodium restriction, knockout mice develop frank hyperkalemia. Finally, in HEK293T cells, exogenous GILZ inhibits NCC activity at least in part by inhibiting SPAK phosphorylation. Thus, GILZ promotes potassium secretion by inhibiting NCC and enhancing distal sodium delivery to the epithelial sodium channel. Additionally, Gilz(-/-) mice have features resembling familial hyperkalemic hypertension, a human disorder that manifests with hyperkalemia associated variably with hypertension. |Animals[MESH] |HEK293 Cells[MESH] |Humans[MESH] |Hyperkalemia/blood[MESH] |Hypertension/metabolism[MESH] |Male[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Minor Histocompatibility Antigens/metabolism[MESH] |Nephrons/*metabolism[MESH] |Phosphorylation[MESH] |Potassium/*blood[MESH] |Protein Serine-Threonine Kinases/metabolism[MESH] |Pseudohypoaldosteronism/*metabolism[MESH] |Renin/blood/metabolism[MESH] |Signal Transduction[MESH] |Sodium Chloride Symporters/drug effects/*metabolism[MESH] |Sodium/*blood[MESH] |Solute Carrier Family 12, Member 3[MESH] |Thiazides/pharmacology[MESH] |Transcription Factors/genetics/*metabolism[MESH]Glucocorticoid-induced leucine zipper protein regulates sodium and pot(epmc).pdf DeepDyve Pubget Overpricing