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10.1152/ajprenal.00396.2011 http://scihub22266oqcxt.onion/10.1152/ajprenal.00396.2011 21900458!3233874!21900458     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21900458&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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 2011 ; 301 (6): F1143-59 Nephropedia Template TP {{tp|p=21900458|t=2011. Molecular regulation of NKCC2 in the thick ascending limb |pdf=|usr=}}{{21900458}} gab.com Text Molecular regulation of NKCC2 in the thick ascending limb JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=21900458 #FOAvip The kidney plays an essential role in blood pressure regulation by controlling short-term and long-term NaCl and water balance. The thick ascending limb of the loop of Henle (TAL) reabsorbs 25-30% of the NaCl filtered by the glomeruli in a process mediated by the apical Na(+)-K(+)-2Cl(-) cotransporter NKCC2, which allows Na(+) and Cl(-) entry from the tubule lumen into TAL cells. In humans, mutations in the gene coding for NKCC2 result in decreased or absent activity characterized by severe salt and volume loss and decreased blood pressure (Bartter syndrome type 1). Opposite to Bartter's syndrome, enhanced NaCl absorption by the TAL is associated with human hypertension and animal models of salt-sensitive hypertension. TAL NaCl reabsorption is subject to exquisite control by hormones like vasopressin, parathyroid, glucagon, and adrenergic agonists (epinephrine and norepinephrine) that stimulate NaCl reabsorption. Atrial natriuretic peptides or autacoids like nitric oxide and prostaglandins inhibit NaCl reabsorption, promoting salt excretion. In general, the mechanism by which hormones control NaCl reabsorption is mediated directly or indirectly by altering the activity of NKCC2 in the TAL. Despite the importance of NKCC2 in renal physiology, the molecular mechanisms by which hormones, autacoids, physical factors, and intracellular ions regulate NKCC2 activity are largely unknown. During the last 5 years, it has become apparent that at least three molecular mechanisms determine NKCC2 activity. As such, membrane trafficking, phosphorylation, and protein-protein interactions have recently been described in TALs and heterologous expression systems as mechanisms that modulate NKCC2 activity. The focus of this review is to summarize recent data regarding NKCC2 regulation and discuss their potential implications in physiological control of TAL function, renal physiology, and blood pressure regulation. Twit Text FOAVip Molecular regulation of NKCC2 in the thick ascending limb ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=21900458 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21900458 #FOAvip English Wikipedia <ref>{{Cite pmid|21900458}}</ref> Molecular regulation of NKCC2 in the thick ascending limb #MMPMID21900458 Ares GR; Caceres PS; Ortiz PA Am J Physiol Renal Physiol 2011[Dec]; 301 (6): F1143-59 PMID21900458show ga The kidney plays an essential role in blood pressure regulation by controlling short-term and long-term NaCl and water balance. The thick ascending limb of the loop of Henle (TAL) reabsorbs 25-30% of the NaCl filtered by the glomeruli in a process mediated by the apical Na(+)-K(+)-2Cl(-) cotransporter NKCC2, which allows Na(+) and Cl(-) entry from the tubule lumen into TAL cells. In humans, mutations in the gene coding for NKCC2 result in decreased or absent activity characterized by severe salt and volume loss and decreased blood pressure (Bartter syndrome type 1). Opposite to Bartter's syndrome, enhanced NaCl absorption by the TAL is associated with human hypertension and animal models of salt-sensitive hypertension. TAL NaCl reabsorption is subject to exquisite control by hormones like vasopressin, parathyroid, glucagon, and adrenergic agonists (epinephrine and norepinephrine) that stimulate NaCl reabsorption. Atrial natriuretic peptides or autacoids like nitric oxide and prostaglandins inhibit NaCl reabsorption, promoting salt excretion. In general, the mechanism by which hormones control NaCl reabsorption is mediated directly or indirectly by altering the activity of NKCC2 in the TAL. Despite the importance of NKCC2 in renal physiology, the molecular mechanisms by which hormones, autacoids, physical factors, and intracellular ions regulate NKCC2 activity are largely unknown. During the last 5 years, it has become apparent that at least three molecular mechanisms determine NKCC2 activity. As such, membrane trafficking, phosphorylation, and protein-protein interactions have recently been described in TALs and heterologous expression systems as mechanisms that modulate NKCC2 activity. The focus of this review is to summarize recent data regarding NKCC2 regulation and discuss their potential implications in physiological control of TAL function, renal physiology, and blood pressure regulation. |Alternative Splicing[MESH] |Animals[MESH] |Blood Pressure/physiology[MESH] |Endocytosis[MESH] |Humans[MESH] |Loop of Henle/*metabolism[MESH] |Mice[MESH] |Phosphorylation[MESH] |Rats[MESH] |Sodium Chloride/metabolism[MESH] |Sodium-Potassium-Chloride Symporters/genetics/*metabolism[MESH]Molecular regulation of NKCC2 in the thick ascending limb (epmc).pdf DeepDyve Pubget Overpricing