ArticlePflugers Archiv : European journal of physiology1994
Properties of inactivation of calcium channel currents in smooth muscle cells of rabbit portal vein.
Article in Pflugers Archiv : European journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Two components of voltage-dependent inactivation in Ca(v)1.2 channels revealed by its gating currents.Biophysical journal · 2003Article
- Prolonged depolarization promotes fast gating kinetics of L-type Ca2+ channels in mouse skeletal myotubes.The Journal of physiology · 2000Article
- Enhanced L-type Ca2+ channel current density in coronary smooth muscle of exercise-trained pigs is compensated to limit myoplasmic free Ca2+ accumulation.The Journal of physiology · 2000Article
- Kinetics of inactivation and restoration from inactivation of the L-type calcium current in human myotubes.The Journal of physiology · 1999Article
- Slow inactivation of tetrodotoxin-insensitive Na+ channels in neurons of rat dorsal root ganglia.The Journal of membrane biology · 1992Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With 10 mM Ba2+ as the charge carrier, inactivation of Ca2+ channel currents could be subdivided into at least two exponentials in smooth muscle cells dispersed from the rabbit portal vein by use of the whole-cell configuration of the patch-clamp technique: fast and slow inactivation. All characteristics of inactivation were independent of the size of the currents. Step changes in the holding potential unveiled an extremely slow recovery and an onset of inactivation of the order of several minutes. Steady-state inactivation critically depended on the duration of the pre-steps. Inactivation curves obtained under steady-state conditions showed as shift by approximately 25 mV towards negative potentials by comparison with curves obtained using 1-s pre-pulses. This shift greatly reduced the window current. Recovery from inactivation studied with double-pulse protocols could be classified into at least two exponentials. The contribution of the slow recovery was accentuated at negative holding potentials. Recovery from inactivation critically depended on the duration of the conditioning voltage step, and was also dependent on the duration of the pre-step: its voltage dependence disappeared when pre-pulses longer than 2 s were applied. Onset of inactivation was composed of at least two exponentials: the fast component was accelerated at less negative pre-step potentials. We propose that several inactivated states are involved in Ca2+ channel inactivation. Transitions between these states are voltage dependent and voltage independent.
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