Literature DB >> 20581043

Kinetic analysis of the effects of H+ or Ni2+ on Kv1.5 current shows that both ions enhance slow inactivation and induce resting inactivation.

Yen May Cheng1, David Fedida, Steven J Kehl.   

Abstract

External H+ and Ni2+ ions inhibit Kv1.5 channels by increasing current decay during a depolarizing pulse and reducing the maximal conductance. Although the former may be attributed to an enhancement of slow inactivation occurring from the open state, the latter cannot. Instead, we propose that the loss of conductance is due to the induction, by H+ or Ni2+, of a resting inactivation process. To assess whether the two inactivation processes are mechanistically related, we examined the time courses for the onset of and recovery from H+- or Ni2+-enhanced slow inactivation and resting inactivation. Compared to the time course of H+- or Ni2+-enhanced slow inactivation at +50 mV, the onset of resting inactivation induced at 80 mV with either ion involves a relatively slower process. Recovery from slow inactivation under control conditions was bi-exponential, indicative of at least two inactivated states. Recovery following H+- or Ni2+-enhanced slow inactivation or resting inactivation had time constants similar to those for recovery from control slow inactivation, although H+ and Ni2+ biased inactivation towards states from which recovery was fast and slow, respectively. The shared time constants suggest that the H+- and Ni2+-enhanced slow inactivated and induced resting inactivated states are similar to those visited during control slow inactivation at pH 7.4. We conclude that in Kv1.5 H+ and Ni2+ differentially enhance a slow inactivation process that involves at least two inactivated states and that resting inactivation is probably a close variant of slow inactivation.

Entities:  

Mesh:

Substances:

Year:  2010        PMID: 20581043      PMCID: PMC2956942          DOI: 10.1113/jphysiol.2010.191544

Source DB:  PubMed          Journal:  J Physiol        ISSN: 0022-3751            Impact factor:   5.182


  41 in total

1.  U-type inactivation of Kv3.1 and Shaker potassium channels.

Authors:  K G Klemic; G E Kirsch; S W Jones
Journal:  Biophys J       Date:  2001-08       Impact factor: 4.033

2.  Effect of external pH on activation of the Kv1.5 potassium channel.

Authors:  Josef G Trapani; Stephen J Korn
Journal:  Biophys J       Date:  2003-01       Impact factor: 4.033

3.  Mechanisms of the inhibition of Shaker potassium channels by protons.

Authors:  John G Starkus; Zoltan Varga; Roland Schönherr; Stefan H Heinemann
Journal:  Pflugers Arch       Date:  2003-08-12       Impact factor: 3.657

4.  Biophysical and molecular mechanisms of Shaker potassium channel inactivation.

Authors:  T Hoshi; W N Zagotta; R W Aldrich
Journal:  Science       Date:  1990-10-26       Impact factor: 47.728

5.  Regulation of a mammalian Shaker-related potassium channel, hKv1.5, by extracellular potassium and pH.

Authors:  H Jäger; S Grissmer
Journal:  FEBS Lett       Date:  2001-01-12       Impact factor: 4.124

6.  Characterization of mibefradil block of the human heart delayed rectifier hKv1.5.

Authors:  L Perchenet; O Clément-Chomienne
Journal:  J Pharmacol Exp Ther       Date:  2000-11       Impact factor: 4.030

7.  External nickel blocks human Kv1.5 channels stably expressed in CHO cells.

Authors:  L Perchenet; O Clément-Chomienne
Journal:  J Membr Biol       Date:  2001-09-01       Impact factor: 1.843

8.  Molecular determinants of the inhibition of human Kv1.5 potassium currents by external protons and Zn(2+).

Authors:  Steven J Kehl; Cyrus Eduljee; Daniel C H Kwan; Shetuan Zhang; David Fedida
Journal:  J Physiol       Date:  2002-05-15       Impact factor: 5.182

9.  The external K+ concentration and mutations in the outer pore mouth affect the inhibition of kv1.5 current by Ni2+.

Authors:  Daniel C H Kwan; Cyrus Eduljee; Logan Lee; Shetuan Zhang; David Fedida; Steven J Kehl
Journal:  Biophys J       Date:  2004-04       Impact factor: 4.033

10.  Molecular coupling of S4 to a K(+) channel's slow inactivation gate.

Authors:  E Loots; E Y Isacoff
Journal:  J Gen Physiol       Date:  2000-11       Impact factor: 4.086

View more
  6 in total

1.  ShakerIR and Kv1.5 mutant channels with enhanced slow inactivation also exhibit K⁺ o-dependent resting inactivation.

Authors:  Yen May Cheng; David Fedida; Steven J Kehl
Journal:  Pflugers Arch       Date:  2013-05-26       Impact factor: 3.657

2.  Molecular determinants of U-type inactivation in Kv2.1 channels.

Authors:  Y M Cheng; J Azer; C M Niven; P Mafi; C R Allard; J Qi; S Thouta; T W Claydon
Journal:  Biophys J       Date:  2011-08-03       Impact factor: 4.033

3.  Regulation of human cardiac Kv1.5 channels by extracellular acidification.

Authors:  Shuang Wang; Wei-Guang Ding; Jia-Yu Bai; Futoshi Toyoda; Min-Jie Wei; Hiroshi Matsuura
Journal:  Pflugers Arch       Date:  2016-10-28       Impact factor: 3.657

4.  Genetic ablation of CaV3.2 channels enhances the arterial myogenic response by modulating the RyR-BKCa axis.

Authors:  Osama F Harraz; Suzanne E Brett; Anil Zechariah; Monica Romero; Jose L Puglisi; Sean M Wilson; Donald G Welsh
Journal:  Arterioscler Thromb Vasc Biol       Date:  2015-06-11       Impact factor: 8.311

5.  Ca(V)3.2 channels and the induction of negative feedback in cerebral arteries.

Authors:  Osama F Harraz; Rasha R Abd El-Rahman; Kamran Bigdely-Shamloo; Sean M Wilson; Suzanne E Brett; Monica Romero; Albert L Gonzales; Scott Earley; Edward J Vigmond; Anders Nygren; Bijoy K Menon; Rania E Mufti; Tim Watson; Yves Starreveld; Tobias Furstenhaupt; Philip R Muellerleile; David T Kurjiaka; Barry D Kyle; Andrew P Braun; Donald G Welsh
Journal:  Circ Res       Date:  2014-08-01       Impact factor: 17.367

6.  Nickel inhibits β-1 adrenoceptor mediated activation of cardiac CFTR chloride channels.

Authors:  Palash P Barman; Hongwei Cheng; Jules C Hancox; Andrew F James
Journal:  Biochem Biophys Res Commun       Date:  2013-01-31       Impact factor: 3.575

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.