Abstract
Potassium countercurrent through the SR K$^+$ channel plays an
important role in Ca$^2+$ release from the SR. To see if Ca$^2+$
regulates the channel, we incorporated canine cardiac SR K$^+$
channel into lipid bilayers. Calcium ions present in either the SR
lumenal (trans) or cytoplasmic (cis) side blocked the cardiac SR
K$^+$ channel in a voltage-dependent manner. When Ca$^2+$
was present on both sides, however, the block appeared to be voltage
independent. A two-binding site model of blockade by an impermeant
divalent cation (Ca$^2+$) can explain this apparent contradiction.
Estimates of SR Ca$^2+$ concentration suggest that under physiological
conditions the cardiac SR K$^+$ channel is partially blocked
by Ca$^2+$ ions present in the lumen of the SR. The reduction
in lumenal Ca$^2+$ during Ca$^2+$ release could increase
K$^+$ conductance.
- 1883938
- animals,
- bilayers,
- biological,
- calcium,
- centrifugation,
- channels,
- cytoplasm,
- density
- dogs,
- electrophoresis,
- gel,
- gov't,
- gradient,
- heart,
- lipid
- mathematics,
- membrane
- models,
- myocardium,
- p.h.s.,
- polyacrylamide
- potassium
- potentials,
- research
- reticulum,
- sarcoplasmic
- solubility,
- support,
- u.s.
Users
Please
log in to take part in the discussion (add own reviews or comments).