Swelling-activated K fluxes in vascular endothelial cells: volume regulation via K-Cl cotransport and K channels
| Autor: | W. C. O'Neill, P. B. Perry |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Osmosis
Potassium Channels Physiology Chlorides Furosemide medicine Animals Bumetanide Ion transporter Fluorescent Dyes Symporters Chemistry Cell Biology Membrane transport Fluoresceins Rubidium Culture Media Endothelial stem cell Hypotonic Solutions Biochemistry Potassium Biophysics Tonicity Endothelium Vascular Efflux Carrier Proteins Cotransporter medicine.drug |
| Zdroj: | American Journal of Physiology-Cell Physiology. 265:C763-C769 |
| ISSN: | 1522-1563 0363-6143 |
| DOI: | 10.1152/ajpcell.1993.265.3.c763 |
| Popis: | K efflux pathways responsible for regulatory volume decrease (RVD) were examined in bovine aortic endothelial cells. Hypotonic swelling produced a rapid and reversible threefold increase in bumetanide-insensitive 86Rb efflux. Swelling-activated 86Rb efflux was inhibited 43% when Cl was replaced with NO3, and this Cl-dependent efflux was inhibited by 1 mM furosemide. Neither Cl replacement nor furosemide inhibited the efflux stimulated by a Ca ionophore (A23187) in isotonic medium. Swelling-activated 86Rb efflux was also inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonate but not by dinitrostilbenedisulfonate. Cell swelling induced a volume-regulatory K loss that was incomplete in hypotonic medium but complete and more rapid when bumetanide was added or when cells were swollen isosmotically. K loss in the presence of bumetanide was partially blocked by furosemide. We conclude that two separate swelling-activated K fluxes mediate RVD in aortic endothelial cells: a Cl-dependent, furosemide-sensitive, but bumetanide-insensitive flux that is consistent with K-Cl cotransport, and a Cl-independent efflux that presumably is mediated by K channels. |
| Databáze: | OpenAIRE |
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