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10.1161/HYPERTENSIONAHA.114.03335 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.114.03335 C4061471!4061471!24799612     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2014 ; 64 (1): 178-84 Nephropedia Template TP {{tp|p=24799612|t=2014. SYMPATHETIC STIMULATION OF THIAZIDE-SENSITIVE SODIUM-CHLORIDE COTRANSPORT IN THE GENERATION OF SALT-SENSITIVE HYPERTENSION |pdf=|usr=}}{{24799612}} gab.com Text SYMPATHETIC STIMULATION OF THIAZIDE-SENSITIVE SODIUM-CHLORIDE COTRANSPORT IN THE GENERATION OF SALT-SENSITIVE HYPERTENSION JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=24799612 #FOAvip Excessive renal efferent sympathetic nerve activity contributes to hypertension in many circumstances. While both hemodynamic and tubular effects likely participate, most evidence supports a major role for ?-adrenergic receptors in mediating the direct epithelial stimulation of sodium retention. Recently, it was reported, however, that norepinephrine activates the thiazide-sensitive transporter, NCC, by stimulating ?-adrenergic receptors. Here, we confirmed this effect and developed an acute adrenergic stimulation model to study the signaling cascade. The results show that norepinephrine increases the abundance of phosphorylated NCC rapidly (161% increase), an effect largely dependent on ?-adrenergic receptors. This effect is not mediated by activation of angiotensin II receptors. We used immunodissected mouse distal convoluted tubule (DCT) to show that DCT cells are especially enriched for ?1-adrenergic receptors, and that the effects of adrenergic stimulation can occur ex vivo (79% increase), suggesting they are direct. As two protein kinases, Ste20p-related Proline Alanine-rich kinase (SPAK) and Oxidative stress responsive 1 (OxSR1), phosphorylate and activate NCC, we examined their roles in norepinephrine effects. Surprisingly, norepinephrine did not affect SPAK abundance or its localization in the DCT; instead, we observed a striking activation of OxSR1. We confirmed that SPAK is not required for NCC activation, using SPAK knockout mice. Together, the data provide strong support for a signaling system involving ?1- receptors in the DCT that activates NCC, at least in part via OxSR1. The results have implications regarding device- and drug-based treatment of hypertension. Twit Text FOAVip SYMPATHETIC STIMULATION OF THIAZIDE-SENSITIVE SODIUM-CHLORIDE COTRANSPORT IN THE GENERATION OF SALT-SENSITIVE HYPERTENSION ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=24799612 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24799612 #FOAvip English Wikipedia <ref>{{Cite pmid|24799612}}</ref> SYMPATHETIC STIMULATION OF THIAZIDE-SENSITIVE SODIUM-CHLORIDE COTRANSPORT IN THE GENERATION OF SALT-SENSITIVE HYPERTENSION #MMPMID24799612 Terker AS; Yang CL; McCormick JA; Meermeier NP; Rogers SL; Grossmann S; Trompf K; Delpire E; Loffing J; Ellison DH Hypertension 2014[Jul]; 64 (1): 178-84 PMID24799612show ga Excessive renal efferent sympathetic nerve activity contributes to hypertension in many circumstances. While both hemodynamic and tubular effects likely participate, most evidence supports a major role for ?-adrenergic receptors in mediating the direct epithelial stimulation of sodium retention. Recently, it was reported, however, that norepinephrine activates the thiazide-sensitive transporter, NCC, by stimulating ?-adrenergic receptors. Here, we confirmed this effect and developed an acute adrenergic stimulation model to study the signaling cascade. The results show that norepinephrine increases the abundance of phosphorylated NCC rapidly (161% increase), an effect largely dependent on ?-adrenergic receptors. This effect is not mediated by activation of angiotensin II receptors. We used immunodissected mouse distal convoluted tubule (DCT) to show that DCT cells are especially enriched for ?1-adrenergic receptors, and that the effects of adrenergic stimulation can occur ex vivo (79% increase), suggesting they are direct. As two protein kinases, Ste20p-related Proline Alanine-rich kinase (SPAK) and Oxidative stress responsive 1 (OxSR1), phosphorylate and activate NCC, we examined their roles in norepinephrine effects. Surprisingly, norepinephrine did not affect SPAK abundance or its localization in the DCT; instead, we observed a striking activation of OxSR1. We confirmed that SPAK is not required for NCC activation, using SPAK knockout mice. Together, the data provide strong support for a signaling system involving ?1- receptors in the DCT that activates NCC, at least in part via OxSR1. The results have implications regarding device- and drug-based treatment of hypertension. äSYMPATHETIC STIMULATION OF THIAZIDE-SENSITIVE SODIUM-CHLORIDE COTRANSP(epmc).pdf DeepDyve Pubget Overpricing