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10.1161/HYPERTENSIONAHA.115.05600 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.05600 C4537321!4537321!26169051     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2015 ; 66 (3): 674-80 Nephropedia Template TP {{tp|p=26169051|t=2015. Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake |pdf=|usr=}}{{26169051}} gab.com Text Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=26169051 #FOAvip Striatin is a protein regulator of vesicular trafficking in neurons that also binds caveolin-1 and Ca2+-calmodulin, and could activate eNOS. We have shown that striatin colocalizes with the mineralocorticoid receptor, and that mineralocorticoid receptor activation increases striatin levels in vascular cells. To test if striatin is a regulator of vascular function, wild-type and heterozygous striatin-deficient mice (Strn+/-) were randomized in crossover intervention to restricted (0.03%) and liberal sodium (1.6%) diets for 7 days on each diet, and blood pressure and aortic vascular function were measured. Compared to wild-type, sodium restriction significantly reduced blood pressure in Strn+/-. On liberal salt intake, phenylephrine and high KCl caused a greater vascular contraction in Strn+/- than wild-type, and endothelium removal, NOS inhibitor L-NAME and guanylate cyclase inhibitor ODQ enhanced phenylephrine contraction to a smaller extent in Strn+/- than WT. On liberal salt, acetylcholine relaxation was less in Strn+/- than wild-type, and endothelium removal, L-NAME and ODQ blocked acetylcholine relaxation, suggesting changes in endothelial NO-cGMP. On liberal salt, eNOS mRNA expression and the ratio of eNOS activator pAkt/total Akt were decreased in Strn+/- versus wild-type. Vascular relaxation to NO donor sodium nitroprusside was not different among groups. Thus striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake. Twit Text FOAVip Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=26169051 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26169051 #FOAvip English Wikipedia <ref>{{Cite pmid|26169051}}</ref> Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake #MMPMID26169051 Garza AE; Pojoga LH; Moize B; Hafiz WM; Opsasnick LA; Siddiqui WT; Horenstein M; Adler GK; Williams GH; Khalil RA Hypertension 2015[Sep]; 66 (3): 674-80 PMID26169051show ga Striatin is a protein regulator of vesicular trafficking in neurons that also binds caveolin-1 and Ca2+-calmodulin, and could activate eNOS. We have shown that striatin colocalizes with the mineralocorticoid receptor, and that mineralocorticoid receptor activation increases striatin levels in vascular cells. To test if striatin is a regulator of vascular function, wild-type and heterozygous striatin-deficient mice (Strn+/-) were randomized in crossover intervention to restricted (0.03%) and liberal sodium (1.6%) diets for 7 days on each diet, and blood pressure and aortic vascular function were measured. Compared to wild-type, sodium restriction significantly reduced blood pressure in Strn+/-. On liberal salt intake, phenylephrine and high KCl caused a greater vascular contraction in Strn+/- than wild-type, and endothelium removal, NOS inhibitor L-NAME and guanylate cyclase inhibitor ODQ enhanced phenylephrine contraction to a smaller extent in Strn+/- than WT. On liberal salt, acetylcholine relaxation was less in Strn+/- than wild-type, and endothelium removal, L-NAME and ODQ blocked acetylcholine relaxation, suggesting changes in endothelial NO-cGMP. On liberal salt, eNOS mRNA expression and the ratio of eNOS activator pAkt/total Akt were decreased in Strn+/- versus wild-type. Vascular relaxation to NO donor sodium nitroprusside was not different among groups. Thus striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake. äCritical Role of Striatin in Blood Pressure and Vascular Responses to (epmc).pdf DeepDyve Pubget Overpricing