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10.1038/sj.bjp.0701630 http://scihub22266oqcxt.onion/10.1038/sj.bjp.0701630 9517376!1565199!9517376     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 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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Br+J+Pharmacol 1998 ; 123 (4): 599-604 Nephropedia Template TP {{tp|p=9517376|t=1998. The inhibitory effect of propranolol on ATP-sensitive potassium channels in neonatal rat heart |pdf=|usr=}}{{9517376}} gab.com Text The inhibitory effect of propranolol on ATP-sensitive potassium channels in neonatal rat heart JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=9517376 #FOAvip 1. Whole cell and single channel recordings of ATP-sensitive K+ current (I(K,ATP)) were carried out in ventricular myocytes isolated from neonatal rat hearts. 2. (+/-)-Propranolol, a commonly used beta-blocker, inhibited the whole cell I(K,ATP) in a concentration-dependent manner with a half-maximal concentration (IC50) of 6.7 +/- 1.4 microM, whereas it blocked the inward rectifier K+ current (I(K,I)) only at much higher concentrations (IC50 = 102.4 +/- 20.2 microM). The inhibition was time- and voltage-independent. 3. In the outside-out patch configuration, (+/-)-propranolol inhibited I(K,ATP) (IC50 = 9.8 +/- 2.9 microM) by decreasing the open probability of the channel without inducing additional noise in the open-channel current or a decrease of single channel conductance. The single channel current of I(K,I) was also blocked by (+/-)-propranolol in the same way as I(K,ATP). 4. (+)-Propranolol, an optic isomer having no beta-blocking effect, inhibited I(K,ATP) (IC50 = 5.8 +/- 1.0 microM), whilst atenolol, a selective beta1-blocker had no effect. Neither GDPbetaS (1 mM) nor GTPgammaS (200 microM) included in the pipette solution modulated the inhibitory effect of (+/-)-propranolol. 5. We concluded that the inhibitory effect of (+/-)-propranolol was not via the beta-adrenergic signal transduction pathway, but by direct inhibition of I(K,ATP) channels. Twit Text FOAVip The inhibitory effect of propranolol on ATP-sensitive potassium channels in neonatal rat heart ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=9517376 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=9517376 #FOAvip English Wikipedia <ref>{{Cite pmid|9517376}}</ref> The inhibitory effect of propranolol on ATP-sensitive potassium channels in neonatal rat heart #MMPMID9517376 Xie LH; Takano M; Noma A Br J Pharmacol 1998[Feb]; 123 (4): 599-604 PMID9517376show ga 1. Whole cell and single channel recordings of ATP-sensitive K+ current (I(K,ATP)) were carried out in ventricular myocytes isolated from neonatal rat hearts. 2. (+/-)-Propranolol, a commonly used beta-blocker, inhibited the whole cell I(K,ATP) in a concentration-dependent manner with a half-maximal concentration (IC50) of 6.7 +/- 1.4 microM, whereas it blocked the inward rectifier K+ current (I(K,I)) only at much higher concentrations (IC50 = 102.4 +/- 20.2 microM). The inhibition was time- and voltage-independent. 3. In the outside-out patch configuration, (+/-)-propranolol inhibited I(K,ATP) (IC50 = 9.8 +/- 2.9 microM) by decreasing the open probability of the channel without inducing additional noise in the open-channel current or a decrease of single channel conductance. The single channel current of I(K,I) was also blocked by (+/-)-propranolol in the same way as I(K,ATP). 4. (+)-Propranolol, an optic isomer having no beta-blocking effect, inhibited I(K,ATP) (IC50 = 5.8 +/- 1.0 microM), whilst atenolol, a selective beta1-blocker had no effect. Neither GDPbetaS (1 mM) nor GTPgammaS (200 microM) included in the pipette solution modulated the inhibitory effect of (+/-)-propranolol. 5. We concluded that the inhibitory effect of (+/-)-propranolol was not via the beta-adrenergic signal transduction pathway, but by direct inhibition of I(K,ATP) channels. |*Potassium Channel Blockers[MESH] |Adenosine Triphosphate/*pharmacology[MESH] |Adrenergic beta-Antagonists/*pharmacology[MESH] |Aging/physiology[MESH] |Animals[MESH] |Animals, Newborn[MESH] |GTP-Binding Proteins/physiology[MESH] |Heart/*drug effects/physiology[MESH] |In Vitro Techniques[MESH] |Potassium Channels/physiology[MESH] |Propranolol/*pharmacology[MESH] |Rats[MESH]The inhibitory effect of propranolol on ATP-sensitive potassium channe(epmc).pdf DeepDyve Pubget Overpricing