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10.1111/bph.13794 http://scihub22266oqcxt.onion/10.1111/bph.13794 C5466521!5466521!28334417     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 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 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28334417.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Br+J+Pharmacol 2017 ; 174 (13): 1972-83 Nephropedia Template TP {{tp|p=28334417|t=2017. Pharmacovigilance database search discloses ClC?K channels as a novel target of the AT1 receptor blockers valsartan and olmesartan |pdf=|usr=}}{{28334417}} gab.com Text Pharmacovigilance database search discloses ClC K channels as a novel target of the AT1 receptor blockers valsartan and olmesartan JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=28334417 #FOAvip Background and Purpose: Human ClC?K chloride channels are highly attractive targets for drug discovery as they have a variety of important physiological functions and are associated with genetic disorders. These channels are crucial in the kidney as they control chloride reabsorption and water diuresis. In addition, loss?of?function mutations of CLCNKB and BSND genes cause Bartter's syndrome (BS), whereas CLCNKA and CLCNKB gain?of?function polymorphisms predispose to a rare form of salt sensitive hypertension. Both disorders lack a personalized therapy that is in most cases only symptomatic. The aim of this study was to identify novel ClC?K ligands from drugs already on the market, by exploiting the pharmacological side activity of drug molecules available from the FDA Adverse Effects Reporting System database. Experimental Approach: We searched for drugs having a Bartter?like syndrome as a reported side effect, with the assumption that BS could be causatively related to the block of ClC?K channels. The ability of the selected BS?causing drugs to bind and block ClC?K channels was then validated through an integrated experimental and computational approach based on patch clamp electrophysiology in HEK293 cells and molecular docking simulations. Key Results: Valsartan and olmesartan were able to block ClC?Ka channels and the molecular requirements for effective inhibition of these channels have been identified. Conclusion and Implications: These results suggest additional mechanisms of action for these sartans further to their primary AT1 receptor antagonism and propose these compounds as leads for designing new potent ClC?K ligands. Twit Text FOAVip Pharmacovigilance database search discloses ClC K channels as a novel target of the AT1 receptor blockers valsartan and olmesartan ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=28334417 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28334417 #FOAvip English Wikipedia <ref>{{Cite pmid|28334417}}</ref> Pharmacovigilance database search discloses ClC?K channels as a novel target of the AT1 receptor blockers valsartan and olmesartan #MMPMID28334417 Imbrici P; Tricarico D; Mangiatordi GF; Nicolotti O; Lograno MD; Conte D; Liantonio A Br J Pharmacol 2017[Jul]; 174 (13): 1972-83 PMID28334417show ga Background and Purpose: Human ClC?K chloride channels are highly attractive targets for drug discovery as they have a variety of important physiological functions and are associated with genetic disorders. These channels are crucial in the kidney as they control chloride reabsorption and water diuresis. In addition, loss?of?function mutations of CLCNKB and BSND genes cause Bartter's syndrome (BS), whereas CLCNKA and CLCNKB gain?of?function polymorphisms predispose to a rare form of salt sensitive hypertension. Both disorders lack a personalized therapy that is in most cases only symptomatic. The aim of this study was to identify novel ClC?K ligands from drugs already on the market, by exploiting the pharmacological side activity of drug molecules available from the FDA Adverse Effects Reporting System database. Experimental Approach: We searched for drugs having a Bartter?like syndrome as a reported side effect, with the assumption that BS could be causatively related to the block of ClC?K channels. The ability of the selected BS?causing drugs to bind and block ClC?K channels was then validated through an integrated experimental and computational approach based on patch clamp electrophysiology in HEK293 cells and molecular docking simulations. Key Results: Valsartan and olmesartan were able to block ClC?Ka channels and the molecular requirements for effective inhibition of these channels have been identified. Conclusion and Implications: These results suggest additional mechanisms of action for these sartans further to their primary AT1 receptor antagonism and propose these compounds as leads for designing new potent ClC?K ligands. äPharmacovigilance database search discloses ClC?K channels as a novel (epmc).pdf DeepDyve Pubget Overpricing