10644524

pubmed:Citation

1

In many nonexcitable cells, hormones and neurotransmitters activate Na(+) influx and mobilize Ca(2+) from intracellular stores. The stores are replenished by Ca(2+) influx via "store-operated" Ca(2+) channels (SOC). The main routes of Na(+) entry in these cells are unresolved, and no role for Na(+) in signaling has been recognized. We demonstrate that the SOC are a major Na(+) entry route in arterial myocytes. Unloading of the Ca(2+) stores with cyclopiazonic acid (a sarcoplasmic reticulum Ca(2+) pump inhibitor) and caffeine induces a large external Na(+)-dependent rise in the cytosolic Na(+) concentration. One component of this rise in cytosolic Na(+) concentration is likely due to Na(+)/Ca(2+) exchange; it depends on elevation of cytosolic Ca(2+) and is insensitive to 10 mM Mg(2+) and 10 microM La(3+). Another component is inhibited by Mg(2+) and La(3+), blockers of SOC; this component persists in cells preloaded with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid to buffer Ca(2+) transients and prevent Na(+)/Ca(2+) exchange-mediated Na(+) entry. This Na(+) entry apparently is mediated by SOC. The Na(+) entry influences Na(+) pump activity and Na(+)/Ca(2+) exchange and has unexpectedly large effects on cell-wide Ca(2+) signaling. The SOC pathway may be a general mechanism by which Na(+) participates in signaling in many types of cells.

eng

IM

MEDLINE

0363-6143

Print

NLM

C163-73

pubmed-meshheading:10644524-Angiotensin II, pubmed-meshheading:10644524-Animals, pubmed-meshheading:10644524-Caffeine, pubmed-meshheading:10644524-Calcium, pubmed-meshheading:10644524-Calcium Channels, L-Type, pubmed-meshheading:10644524-Calcium Signaling, pubmed-meshheading:10644524-Cardiotonic Agents, pubmed-meshheading:10644524-Cells, Cultured, pubmed-meshheading:10644524-Chelating Agents, pubmed-meshheading:10644524-Cytosol, pubmed-meshheading:10644524-Dinucleoside Phosphates, pubmed-meshheading:10644524-Egtazic Acid, pubmed-meshheading:10644524-Enzyme Activation, pubmed-meshheading:10644524-Enzyme Inhibitors, pubmed-meshheading:10644524-Extracellular Space, pubmed-meshheading:10644524-Female, pubmed-meshheading:10644524-Fluorescent Dyes, pubmed-meshheading:10644524-Fura-2, pubmed-meshheading:10644524-Indoles, pubmed-meshheading:10644524-Magnesium, pubmed-meshheading:10644524-Mesenteric Arteries, pubmed-meshheading:10644524-Muscle, Smooth, Vascular, pubmed-meshheading:10644524-Ouabain, pubmed-meshheading:10644524-Phenylephrine, pubmed-meshheading:10644524-Phosphodiesterase Inhibitors, pubmed-meshheading:10644524-Rats, pubmed-meshheading:10644524-Rats, Sprague-Dawley, pubmed-meshheading:10644524-Sarcoplasmic Reticulum, pubmed-meshheading:10644524-Sodium, pubmed-meshheading:10644524-Sodium-Calcium Exchanger, pubmed-meshheading:10644524-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:10644524-Vasoconstrictor Agents

Na(+) entry via store-operated channels modulates Ca(2+) signaling in arterial myocytes.

Journal Article, Research Support, U.S. Gov't, P.H.S.