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10.1172/JCI24134 http://scihub22266oqcxt.onion/10.1172/JCI24134 C1090474!1090474 !15902302     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15902302 &cmd=llinks): Failed to open stream: HTTP request failed! 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Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia |pdf=|usr=}}{{15902302 }} gab.com Text Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=15902302 #FOAvip Thiazide diuretics enhance renal Na+ excretion by blocking the Na+-Cl- cotransporter (NCC), and mutations in NCC result in Gitelman syndrome. The mechanisms underlying the accompanying hypocalciuria and hypomagnesemia remain debated. Here, we show that enhanced passive Ca2+ transport in the proximal tubule rather than active Ca2+ transport in distal convolution explains thiazide-induced hypocalciuria. First, micropuncture experiments in mice demonstrated increased reabsorption of Na+ and Ca2+ in the proximal tubule during chronic hydrochlorothiazide (HCTZ) treatment, whereas Ca2+ reabsorption in distal convolution appeared unaffected. Second, HCTZ administration still induced hypocalciuria in transient receptor potential channel subfamily V, member 5-knockout (Trpv5-knockout) mice, in which active distal Ca2+ reabsorption is abolished due to inactivation of the epithelial Ca2+ channel Trpv5. Third, HCTZ upregulated the Na+/H+ exchanger, responsible for the majority of Na+ and, consequently, Ca2+ reabsorption in the proximal tubule, while the expression of proteins involved in active Ca2+ transport was unaltered. Fourth, experiments addressing the time-dependent effect of a single dose of HCTZ showed that the development of hypocalciuria parallels a compensatory increase in Na+ reabsorption secondary to an initial natriuresis. Hypomagnesemia developed during chronic HCTZ administration and in NCC-knockout mice, an animal model of Gitelman syndrome, accompanied by downregulation of the epithelial Mg2+ channel transient receptor potential channel subfamily M, member 6 (Trpm6). Thus, Trpm6 downregulation may represent a general mechanism involved in the pathogenesis of hypomagnesemia accompanying NCC inhibition or inactivation. Twit Text FOAVip Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=15902302 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15902302 #FOAvip English Wikipedia <ref>{{Cite pmid|15902302 }}</ref> Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia #MMPMID15902302 Nijenhuis T ; Vallon V ; van der Kemp AW ; Loffing J ; Hoenderop JG ; Bindels RJ J Clin Invest 2005[Jun]; 115 (6 ): 1651-8 PMID15902302 show ga Thiazide diuretics enhance renal Na+ excretion by blocking the Na+-Cl- cotransporter (NCC), and mutations in NCC result in Gitelman syndrome. The mechanisms underlying the accompanying hypocalciuria and hypomagnesemia remain debated. Here, we show that enhanced passive Ca2+ transport in the proximal tubule rather than active Ca2+ transport in distal convolution explains thiazide-induced hypocalciuria. First, micropuncture experiments in mice demonstrated increased reabsorption of Na+ and Ca2+ in the proximal tubule during chronic hydrochlorothiazide (HCTZ) treatment, whereas Ca2+ reabsorption in distal convolution appeared unaffected. Second, HCTZ administration still induced hypocalciuria in transient receptor potential channel subfamily V, member 5-knockout (Trpv5-knockout) mice, in which active distal Ca2+ reabsorption is abolished due to inactivation of the epithelial Ca2+ channel Trpv5. Third, HCTZ upregulated the Na+/H+ exchanger, responsible for the majority of Na+ and, consequently, Ca2+ reabsorption in the proximal tubule, while the expression of proteins involved in active Ca2+ transport was unaltered. Fourth, experiments addressing the time-dependent effect of a single dose of HCTZ showed that the development of hypocalciuria parallels a compensatory increase in Na+ reabsorption secondary to an initial natriuresis. Hypomagnesemia developed during chronic HCTZ administration and in NCC-knockout mice, an animal model of Gitelman syndrome, accompanied by downregulation of the epithelial Mg2+ channel transient receptor potential channel subfamily M, member 6 (Trpm6). Thus, Trpm6 downregulation may represent a general mechanism involved in the pathogenesis of hypomagnesemia accompanying NCC inhibition or inactivation. |Animals [MESH] |Benzothiadiazines [MESH] |Calcium Channels/genetics/metabolism [MESH] |Calcium Metabolism Disorders/chemically induced/metabolism/pathology [MESH] |Calcium/*metabolism [MESH] |Disease Models, Animal [MESH] |Diuretics [MESH] |Down-Regulation [MESH] |Humans [MESH] |Ion Transport/genetics [MESH] |Kidney Tubules, Proximal/*metabolism/pathology [MESH] |Magnesium/*metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Renal Tubular Transport, Inborn Errors/genetics/*metabolism/pathology [MESH] |Sodium Chloride Symporter Inhibitors/toxicity [MESH] |Sodium-Hydrogen Exchangers/genetics/metabolism [MESH] |Sodium-Potassium-Chloride Symporters/genetics/*metabolism [MESH] |TRPV Cation Channels [MESH] |Up-Regulation [MESH]Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance (epmc).pdf DeepDyve Pubget Overpricing