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10.3389/fphar.2010.00144 http://scihub22266oqcxt.onion/10.3389/fphar.2010.00144 21833183!3153018!21833183     free     free     free 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       Front+Pharmacol 2010 ; 1 (ä): 144 Nephropedia Template TP {{tp|p=21833183|t=2010. Propranolol blocks cardiac and neuronal voltage-gated sodium channels |pdf=|usr=}}{{21833183}} gab.com Text Propranolol blocks cardiac and neuronal voltage-gated sodium channels JO: Front Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=21833183 #FOAvip Propranolol is a widely used, non-selective beta-adrenergic receptor antagonist with proven efficacy in treating cardiovascular disorders and in the prevention of migraine headaches. At plasma concentrations exceeding those required for beta-adrenergic receptor inhibition, propranolol also exhibits anti-arrhythmic ("membrane stabilizing") effects that are not fully explained by beta-blockade. Previous in vitro studies suggested that propranolol may have local anesthetic effects. We directly tested the effects of propranolol on heterologously expressed recombinant human cardiac (NaV1.5) and brain (NaV1.1, NaV1.2, NaV1.3) sodium channels using whole-cell patch-clamp recording. We found that block was not stereospecific as we observed approximately equal IC50 values for tonic and use-dependent block by R-(+) and S-(-) propranolol (tonic block: R: 21.4 muM vs S: 23.6 muM; use-dependent block: R: 2.7 muM vs S: 2.6 muM). Metoprolol and nadolol did not block NaV1.5 indicating that sodium channel block is not a class effect of beta-blockers. The biophysical effects of R-(+)-propranolol on NaV1.5 and NaV1.1 resembled that of the prototypical local anesthetic lidocaine including the requirement for a critical phenylalanine residue (F1760 in NaV1.5) in the domain 4 S6 segment. Finally, we observed that brain sodium channels exhibited less sensitivity to R-(+)-propranolol than NaV1.5 channels. Our findings establish sodium channels as targets for propranolol and may help explain some beneficial effects of the drug in treating cardiac arrhythmias, and may explain certain adverse central nervous system effects. Twit Text FOAVip Propranolol blocks cardiac and neuronal voltage-gated sodium channels ????Front Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=21833183 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21833183 #FOAvip English Wikipedia <ref>{{Cite pmid|21833183}}</ref> Propranolol blocks cardiac and neuronal voltage-gated sodium channels #MMPMID21833183 Wang DW; Mistry AM; Kahlig KM; Kearney JA; Xiang J; George AL Jr Front Pharmacol 2010[]; 1 (ä): 144 PMID21833183show ga Propranolol is a widely used, non-selective beta-adrenergic receptor antagonist with proven efficacy in treating cardiovascular disorders and in the prevention of migraine headaches. At plasma concentrations exceeding those required for beta-adrenergic receptor inhibition, propranolol also exhibits anti-arrhythmic ("membrane stabilizing") effects that are not fully explained by beta-blockade. Previous in vitro studies suggested that propranolol may have local anesthetic effects. We directly tested the effects of propranolol on heterologously expressed recombinant human cardiac (NaV1.5) and brain (NaV1.1, NaV1.2, NaV1.3) sodium channels using whole-cell patch-clamp recording. We found that block was not stereospecific as we observed approximately equal IC50 values for tonic and use-dependent block by R-(+) and S-(-) propranolol (tonic block: R: 21.4 muM vs S: 23.6 muM; use-dependent block: R: 2.7 muM vs S: 2.6 muM). Metoprolol and nadolol did not block NaV1.5 indicating that sodium channel block is not a class effect of beta-blockers. The biophysical effects of R-(+)-propranolol on NaV1.5 and NaV1.1 resembled that of the prototypical local anesthetic lidocaine including the requirement for a critical phenylalanine residue (F1760 in NaV1.5) in the domain 4 S6 segment. Finally, we observed that brain sodium channels exhibited less sensitivity to R-(+)-propranolol than NaV1.5 channels. Our findings establish sodium channels as targets for propranolol and may help explain some beneficial effects of the drug in treating cardiac arrhythmias, and may explain certain adverse central nervous system effects. äPropranolol blocks cardiac and neuronal voltage-gated sodium channels (epmc).pdf DeepDyve Pubget Overpricing