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10.1161/HYPERTENSIONAHA.115.07032 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.07032 C4802158!4802158!26883268     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2016 ; 67 (4): 792-9 Nephropedia Template TP {{tp|p=26883268|t=2016. Inhibition of NOS1 induces salt-sensitive hypertension in NOS1? knockout and wild type mice |pdf=|usr=}}{{26883268}} gab.com Text Inhibition of NOS1 induces salt-sensitive hypertension in NOS1 knockout and wild type mice JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=26883268 #FOAvip We recently shown that ?, ?, and ? splice variants of neuronal nitric oxide synthase (NOS1) expressed in the macula densa and NOS1? accounts for most of the NO generation. We have also demonstrated that the mice with deletion of NOS1 specifically from the macula densa developed salt-sensitive hypertension. However, the global NOS1KO strain is not hypertensive nor salt-sensitive. This global NOS1KO strain is actually a NOS1?KO model. Consequently, we hypothesized that inhibition of NOS1? in NOS1?KO mice induces salt-sensitive hypertension.NOS1?KO and C57BL/6 WT mice were implanted with telemetry transmitters and divided into 7-nitroindazole (7-NI) (10mg/kg/day)-treated and non-treated groups. All of the mice were fed a normal salt (0.4% NaCl) diet for 5 days, followed by a high salt diet (4%NaCl). NO generation by the macula densa was inhibited by over 90% in WT and NOS1?KO mice treated with 7-NI. GFR in conscious mice was increased by about 40% following a high salt diet in both NOS1?KO and WT mice. In response to acute volume expansion, GFR, diuretic and natriuretic response were significantly blunted in the WT and KO mice treated with 7-NI. Mean arterial pressure had no significant changes in mice fed a high salt diet, but increased about 15 mmHg similarly in NOS1?KO and WT mice treated with 7-NI.We conclude that NOS1?, but not NOS1? plays an important role in control of sodium excretion and hemodynamics in response to either an acute or a chronic salt loading. Twit Text FOAVip Inhibition of NOS1 induces salt-sensitive hypertension in NOS1 knockout and wild type mice ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=26883268 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26883268 #FOAvip English Wikipedia <ref>{{Cite pmid|26883268}}</ref> Inhibition of NOS1 induces salt-sensitive hypertension in NOS1? knockout and wild type mice #MMPMID26883268 Wang X; Chandrashekar K; Wang L; Lai EY; Wei J; Zhang G; Wang S; Zhang J; Juncos LA; Liu R Hypertension 2016[Apr]; 67 (4): 792-9 PMID26883268show ga We recently shown that ?, ?, and ? splice variants of neuronal nitric oxide synthase (NOS1) expressed in the macula densa and NOS1? accounts for most of the NO generation. We have also demonstrated that the mice with deletion of NOS1 specifically from the macula densa developed salt-sensitive hypertension. However, the global NOS1KO strain is not hypertensive nor salt-sensitive. This global NOS1KO strain is actually a NOS1?KO model. Consequently, we hypothesized that inhibition of NOS1? in NOS1?KO mice induces salt-sensitive hypertension.NOS1?KO and C57BL/6 WT mice were implanted with telemetry transmitters and divided into 7-nitroindazole (7-NI) (10mg/kg/day)-treated and non-treated groups. All of the mice were fed a normal salt (0.4% NaCl) diet for 5 days, followed by a high salt diet (4%NaCl). NO generation by the macula densa was inhibited by over 90% in WT and NOS1?KO mice treated with 7-NI. GFR in conscious mice was increased by about 40% following a high salt diet in both NOS1?KO and WT mice. In response to acute volume expansion, GFR, diuretic and natriuretic response were significantly blunted in the WT and KO mice treated with 7-NI. Mean arterial pressure had no significant changes in mice fed a high salt diet, but increased about 15 mmHg similarly in NOS1?KO and WT mice treated with 7-NI.We conclude that NOS1?, but not NOS1? plays an important role in control of sodium excretion and hemodynamics in response to either an acute or a chronic salt loading. äInhibition of NOS1 induces salt-sensitive hypertension in NOS1? knocko(epmc).pdf DeepDyve Pubget Overpricing