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10.1038/ki.1996.426 http://scihub22266oqcxt.onion/10.1038/ki.1996.426 8887276!ä!8887276 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kidney+Int 1996 ; 50 (4): 1180-90 Nephropedia Template TP {{tp|p=8887276|t=1996. Thiazide treatment of rats provokes apoptosis in distal tubule cells |pdf=|usr=}}{{8887276}} gab.com Text Thiazide treatment of rats provokes apoptosis in distal tubule cells JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=8887276 #FOAvip We studied the effects of inhibition of apical NaCl entry on the structural correlates for electrolyte transport in the distal convoluted tubule (DCT) of rats. Thiazide diuretics were used to block NaCl entry specifically in the DCT. Metolazone or hydrochlorothiazide (HCTZ) were applied for three days subcutaneously via osmotic minipumps. The renal epithelial structure of control and treated rats was studied by light and electron microscopy. Distribution of the thiazide-sensitive NaCl cotransporter (rTSC1), calbindin D28K and Ca(2+)-Mg(2+)-ATPase was examined by immunohistochemistry, and the content of rTSC1 transcripts by Northern blot and in situ hybridization. In treated rats the DCT epithelium had lost the structural characteristics of electrolyte transporting epithelia and the cells were in different stages of apoptosis. In damaged cells calbindin D28K and Ca(2+)-Mg(2+)-ATPase were strongly decreased; the rTSC1 was shifted from the luminal membrane to the basal cell half and was found additionally in small membrane vesicles in intercellular and peritubular spaces. Transcripts of rTSC1 were drastically reduced in homogenates of kidney cortex and almost absent in damaged DCT cells. All other tubular segments were unaffected by the treatment. Focal inflammatory infiltrates were found to be specifically surrounding DCT profiles. Thus, inhibition by thiazides of apical NaCl entry into DCT cells is associated with apoptosis of DCT cells and focal peritubular inflammation. Twit Text FOAVip Thiazide treatment of rats provokes apoptosis in distal tubule cells ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=8887276 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=8887276 #FOAvip English Wikipedia <ref>{{Cite pmid|8887276}}</ref> Thiazide treatment of rats provokes apoptosis in distal tubule cells #MMPMID8887276 Loffing J; Loffing-Cueni D; Hegyi I; Kaplan MR; Hebert SC; Le Hir M; Kaissling B Kidney Int 1996[Oct]; 50 (4): 1180-90 PMID8887276show ga We studied the effects of inhibition of apical NaCl entry on the structural correlates for electrolyte transport in the distal convoluted tubule (DCT) of rats. Thiazide diuretics were used to block NaCl entry specifically in the DCT. Metolazone or hydrochlorothiazide (HCTZ) were applied for three days subcutaneously via osmotic minipumps. The renal epithelial structure of control and treated rats was studied by light and electron microscopy. Distribution of the thiazide-sensitive NaCl cotransporter (rTSC1), calbindin D28K and Ca(2+)-Mg(2+)-ATPase was examined by immunohistochemistry, and the content of rTSC1 transcripts by Northern blot and in situ hybridization. In treated rats the DCT epithelium had lost the structural characteristics of electrolyte transporting epithelia and the cells were in different stages of apoptosis. In damaged cells calbindin D28K and Ca(2+)-Mg(2+)-ATPase were strongly decreased; the rTSC1 was shifted from the luminal membrane to the basal cell half and was found additionally in small membrane vesicles in intercellular and peritubular spaces. Transcripts of rTSC1 were drastically reduced in homogenates of kidney cortex and almost absent in damaged DCT cells. All other tubular segments were unaffected by the treatment. Focal inflammatory infiltrates were found to be specifically surrounding DCT profiles. Thus, inhibition by thiazides of apical NaCl entry into DCT cells is associated with apoptosis of DCT cells and focal peritubular inflammation. |*Benzothiadiazines[MESH] |*Symporters[MESH] |Analysis of Variance[MESH] |Animals[MESH] |Apoptosis/*physiology[MESH] |Ca(2+) Mg(2+)-ATPase/analysis[MESH] |Calbindin 1[MESH] |Calbindins[MESH] |Carrier Proteins/analysis[MESH] |Diuretics[MESH] |Fluorescent Antibody Technique, Indirect[MESH] |Immunohistochemistry[MESH] |In Situ Hybridization[MESH] |Kidney Tubules, Distal/drug effects/*pathology[MESH] |Kidney/pathology/ultrastructure[MESH] |Male[MESH] |Microscopy, Electron[MESH] |RNA/analysis[MESH] |Rats[MESH] |Rats, Wistar[MESH] |Receptors, Drug/analysis[MESH] |S100 Calcium Binding Protein G/analysis[MESH] |Sodium Chloride Symporter Inhibitors/analysis/*pharmacology[MESH] |Sodium Chloride Symporters[MESH]Thiazide treatment of rats provokes apoptosis in distal tubule cells (epmc).pdf DeepDyve Pubget Overpricing