title: Blockade of cardiac sarcoplasmic reticulum K+ channel by Ca2+: two-binding-site model of blockade.
abstract: Potassium countercurrent through the SR K+ channel plays an important role in Ca2+ release from the SR. To see if Ca2+ 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 Ca2+ 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 (Ca2+) can explain this apparent contradiction. Estimates of SR Ca2+ concentration suggest that under physiological conditions the cardiac SR K+ channel is partially blocked by Ca2+ ions present in the lumen of the SR. The reduction in lumenal [Ca2+] during Ca2+ release could increase K+ conductance.
authors.affiliation: Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710.
authors.forename: Q Y
authors.initials: QY
authors.lastname: Liu
authors.forename: H C
authors.initials: HC
authors.lastname: Strauss
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D003593:Cytoplasm / Q000502:physiology; D004285:Dogs; D006321:Heart / Q000502:physiology*; D008051:Lipid Bilayers; D008433:Mathematics; D008564:Membrane Potentials; D008954:Models, Biological; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000502:physiology*
chemical_list: D008051:Lipid Bilayers; D015221:Potassium Channels; D002118:Calcium