ArticleThe Journal of physiology2010
Quinidine interaction with Shab K+ channels: pore block and irreversible collapse of the K+ conductance.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Conductance stability and Na+ interaction with Shab K+ channels under low K+ conditions.Channels (Austin, Tex.) · 2021Article
- Dronedarone blockage of the tumor-related Kv10.1 channel: a comparison with amiodarone.Pflugers Archiv : European journal of physiology · 2020Article
- Mibefradil inhibition of the Cole-Moore shift and KChannels (Austin, Tex.) · 2017Article
- Article
- Voltage-dependent biphasic effects of chloroquine on delayed rectifier K(+)-channel currents in murine thymocytes.The journal of physiological sciences : JPS · 2012Article
- A model of the interaction between N-type and C-type inactivation in Kv1.4 channels.Biophysical journal · 2011Article
- Interaction of local anesthetics with the K (+) channel pore domain: KcsA as a model for drug-dependent tetramer stability.Channels (Austin, Tex.)Article
- Shab K (+) channel slow inactivation: a test for U-type inactivation and a hypothesis regarding K (+) -facilitated inactivation mechanisms.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Quinidine is a commonly used antiarrhythmic agent and a tool to study ion channels. Here it is reported that quinidine equilibrates within seconds across the Sf9 plasma membrane, blocking the open pore of Shab channels from the intracellular side of the membrane in a voltage-dependent manner with 1:1 stoichiometry. On binding to the channels, quinidine interacts with pore K(+) ions in a mutually destabilizing manner. As a result, when the channels are blocked by quinidine with the cell bathed in an external medium lacking K(+), the Shab conductance G(K) collapses irreversibly, despite the presence of a physiological [K(+)] in the intracellular solution. The quinidine-promoted collapse of Shab G(K) resembles the collapse of Shaker G(K) observed with 0 K(+) solutions on both sides of the membrane: thus the extent of G(K) drop depends on the number of activating pulses applied in the presence of quinidine, but is independent of the pulse duration. Taken together the observations indicate that, as in Shaker, the quinidine-promoted collapse of Shab G(K) occurs during deactivation of the channels, at the end of each activating pulse, with a probability of 0.1 per pulse at 80 mV. It appears that when Shab channels are open, the pore conformation able to conduct is stable in the absence of K(+), but on deactivation this conformation collapses irreversibly.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.