title: Phosphate ion channels in sarcoplasmic reticulum of rabbit skeletal muscle.
abstract: 1. Phosphate ions (P(i)) enter intracellular Ca2+ stores and precipitate Ca2+. Since transport pathways for P(i) across the membrane of intracellular calcium stores have not been identified and anion channels could provide such a pathway, we have examined the P(i) conductance of single anion channels from the sarcoplasmic reticulum (SR) of rabbit skeletal muscle using the lipid bilayer technique. 2. Two anion channels in skeletal muscle SR, the small conductance (SCl) and big conductance (BCl) chloride channels, were both found to have a P(i) conductance of 10 pS in 50 mM P(i). The SCl channel is a divalent anion channel which can pass HPO4(2-) as well as SO4(2-) (60 pS in 100 mM free SO4(2-)). The BCl channel is primarily a monovalent anion channel. The SCl and BCl channels are permeable to a number of small monovalent anions, showing minor selectivity between Cl-, I- and Br- (Cl- > I- > Br-) and relative impermeability to cations and large polyatomic anions (Cs+, Na+, choline+, Tris+, Hepes- and CH3O3S-). 3. The P(i) conductance of SCl and BCl channels suggests that both channel types could sustain the observed P(i) fluxes across the SR membrane. Comparison of the blocking effects of the phosphonocarboxylic acids, ATP and DIDS, on the anion channels with their effects on P(i) transport suggests that the SCl channel is the more likely candidate for the SR P(i) transport mechanism. 4. The SCl channel, with previously unknown function, provides a regulated pathway for P(i) across the SR membrane which would promote P(i) entry and thereby changes in the rapidly releasable Ca2+ store during onset and recovery from muscle fatigue. Anion channels may provide a pathway for P(i) movement into and out of Ca2+ stores in general.
authors.affiliation: School of Biochemistry and Molecular Biology, Faculty of Science, Australian National University, Canberra, ACT 0200, Australia. derek.laver@anu.edu.a
authors.forename: D R
authors.initials: DR
authors.lastname: Laver
authors.forename: G K
authors.initials: GK
authors.lastname: Lenz
authors.forename: A F
authors.initials: AF
authors.lastname: Dulhunty
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000465:Algorithms; D000818:Animals; D001693:Biological Transport, Active / Q000502:physiology; D002586:Cesium / Q000494:pharmacology; D018118:Chloride Channels / Q000187:drug effects / Q000378:metabolism; D002712:Chlorides / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D010710:Phosphates / Q000378:metabolism*; D011817:Rabbits; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism*
chemical_list: D018118:Chloride Channels; D002712:Chlorides; D007473:Ion Channels; D010710:Phosphates; D002586:Cesium; C028019:cesium chloride; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid