Abstract
A new kind of chloride channels in the cardiac sarcoplasmic reticulum,
116 pS Cl$^-$ channel (500 mM Cl$^-$ in the cis and 50 mM
Cl$^-$ in the trans chamber solutions), which is activated by
protein-kinase-A-dependent phosphorylation, has been determined to
conduct adenine nucleotide as a transporter between cytosol and SR
lumen. We investigated the voltage-dependent gating of this Cl$^-$
channel by recording single-channel activities using the planar lipid
bilayer-vesicle fusion technique. The channel activities did not
change at different membrane potentials (-100 mV to +50 mV) or different
Ca$^2+$ concentrations (1 nM to 1 mM) in cis solution. In the
presence of calmodulin (CaM) (0.1 microM /microg SR vesicles), however,
Ca$^2+$ added to the cis solution at 0 mV inhibited channel openings
in a Ca$^2+$ -concentration-dependent manner. These effects were
prevented by the addition of CaM inhibitors. The blocking effects
of CaM differed depending on the membrane potentials at negative
potentials below -20 mV. With CaM and 3 microM Ca$^2+$, the values
of opening probability were 0 at -80 mV, 0.2 at -40 mV, 0.3 at -20
mV, 0.71 at 0 mV and 0.92 at +20 mV. These results may indicate the
membrane potential affects the action of Ca$^2+$ /CaM complex
- acidosis,
- action
- adipocytes,
- adolescent,
- adrenergic
- adult,
- agents,
- and
- animals,
- anti-arrhythmia
- arrhythmia,
- atpase,
- atrial,
- base
- beta-agonists,
- biological
- biological,
- block,
- blockers,
- body
- bone
- bundle-branch
- calcium
- calcium,
- calcium-activated,
- calmodulin,
- cardiac,
- cardiomyopathies,
- cation
- cell
- cells,
- channel
- channels,
- child,
- chloride
- comparative
- concentration,
- conduction
- conductivity,
- confocal,
- cos
- cultured,
- cytoplasmic
- defects,
- differentiation,
- dna
- dna-binding
- dominant,
- electric
- electrocardiography,
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