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10.1161/CIRCRESAHA.115.304110 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.115.304110 C4116673!4116673!24903104     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24903104&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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Res 2014 ; 115 (3): 388-99 Nephropedia Template TP {{tp|p=24903104|t=2014. At2 Receptor Activation Induces Natriuresis and Lowers Blood Pressure |pdf=|usr=}}{{24903104}} gab.com Text At2 Receptor Activation Induces Natriuresis and Lowers Blood Pressure JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=24903104 #FOAvip Rationale: Compound 21 (C-21) is a highly selective non-peptide AT2 receptor (AT2R) agonist. Objective: To test the hypothesis that renal proximal tubule AT2Rs induce natriuresis and lower blood pressure (BP) in Sprague-Dawley rats and mice. Methods and Results: In rats, AT2R activation with intravenous C-21 increased urinary sodium (Na+) excretion (UNaV) by 10-fold (P<0.0001); this natriuresis was abolished by direct renal interstitial (RI) infusion of specific AT2R antagonist PD-123319 (PD). C-21 increased fractional excretion of Na+ (FENa; P<0.05) and lithium (FELi; P<0.01) without altering renal hemodynamic function. AT2R activation increased renal proximal tubule cell (RPTC) apical membrane AT2R protein (P<0.001) without changing total AT2R expression and internalized/inactivated Na+- H+ exchanger-3 (NHE-3) and Na+/K+ATPase (NKA). C-21-induced natriuresis was accompanied by an increase in RI cyclic GMP (cGMP; P<0.01); C-21-induced increases in UNaV and RI cGMP were abolished by RI nitric oxide (NO) synthase inhibitor L-NAME or bradykinin (BK) B2 receptor antagonist icatibant. Renal AT2R activation with C-21 prevented Na+ retention and lowered BP in the angiotensin II (Ang II) infusion model of experimental hypertension. Conclusions: AT2R activation initiates its translocation to the RPTC apical membrane and the internalization of NHE-3 and NKA inducing natriuresis in a BK-NO-cGMP-dependent manner. Intrarenal AT2R activation prevents Na+ retention and lowers BP in Ang II-dependent hypertension. AT2R activation holds promise as a RPT natriuretic/diuretic target for the treatment of fluid retaining states and hypertension. Twit Text FOAVip At2 Receptor Activation Induces Natriuresis and Lowers Blood Pressure ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=24903104 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24903104 #FOAvip English Wikipedia <ref>{{Cite pmid|24903104}}</ref> At2 Receptor Activation Induces Natriuresis and Lowers Blood Pressure #MMPMID24903104 Kemp BA; Howell NL; Gildea JJ; Keller SR; Padia SH; Carey RM Circ Res 2014[Jul]; 115 (3): 388-99 PMID24903104show ga Rationale: Compound 21 (C-21) is a highly selective non-peptide AT2 receptor (AT2R) agonist. Objective: To test the hypothesis that renal proximal tubule AT2Rs induce natriuresis and lower blood pressure (BP) in Sprague-Dawley rats and mice. Methods and Results: In rats, AT2R activation with intravenous C-21 increased urinary sodium (Na+) excretion (UNaV) by 10-fold (P<0.0001); this natriuresis was abolished by direct renal interstitial (RI) infusion of specific AT2R antagonist PD-123319 (PD). C-21 increased fractional excretion of Na+ (FENa; P<0.05) and lithium (FELi; P<0.01) without altering renal hemodynamic function. AT2R activation increased renal proximal tubule cell (RPTC) apical membrane AT2R protein (P<0.001) without changing total AT2R expression and internalized/inactivated Na+- H+ exchanger-3 (NHE-3) and Na+/K+ATPase (NKA). C-21-induced natriuresis was accompanied by an increase in RI cyclic GMP (cGMP; P<0.01); C-21-induced increases in UNaV and RI cGMP were abolished by RI nitric oxide (NO) synthase inhibitor L-NAME or bradykinin (BK) B2 receptor antagonist icatibant. Renal AT2R activation with C-21 prevented Na+ retention and lowered BP in the angiotensin II (Ang II) infusion model of experimental hypertension. Conclusions: AT2R activation initiates its translocation to the RPTC apical membrane and the internalization of NHE-3 and NKA inducing natriuresis in a BK-NO-cGMP-dependent manner. Intrarenal AT2R activation prevents Na+ retention and lowers BP in Ang II-dependent hypertension. AT2R activation holds promise as a RPT natriuretic/diuretic target for the treatment of fluid retaining states and hypertension. äAt2 Receptor Activation Induces Natriuresis and Lowers Blood Pressure (epmc).pdf DeepDyve Pubget Overpricing