A1 Refereed original research article in a scientific journal
REGULATORY VOLUME DECREASE IN LAMPREY ERYTHROCYTES - MECHANISMS OF K+ AND CL- LOSS
Authors: VIRKKI LV, NIKINMAA M
Publisher: AMER PHYSIOLOGICAL SOC
Publication year: 1995
Journal: AJP - Regulatory, Integrative and Comparative Physiology
Journal name in source: AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Journal acronym: AM J PHYSIOL-REG I
Volume: 268
Issue: 3
First page : R590
Last page: R597
Number of pages: 8
ISSN: 0363-6119
Abstract
The nature of the swelling-activated K+ and Cl- transport pathways of lamprey (Lampetra fluviatilis) erythrocytes was studied. In isosmotic medium, unidirectional K+ and Cl- effluxes appear to be largely mediated by conductive pathways. Unidirectional Cl- efflux increased as a function of a decrease in medium osmolarity. The swelling-activated Cl- transport was inhibited by R(+)-[(2-n-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo- 1H-inden-5-yl)oxy]acetic acid (DIOA), furosemide, and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In contrast, moderate cell swelling did not increase unidirectional ouabain-insensitive K+ efflux. However, inhibition of transport by Ba2+ was markedly reduced. This suggests that the Ba2+-sensitive pathway that mediated most of the K+ efflux in isosmotic conditions was inhibited by cell swelling and a Ba2+-insensitive pathway was activated. DIOA had no effect on K+ efflux in isosmotic or hyposmotic medium. These data and the finding that substitution of NO3- or SCN- for Cl- had only a minor effect on the swelling-induced net extrusion of K+ and water indicate that the pathways for K+ and Cl-, activated by cell swelling, are conductive.
The nature of the swelling-activated K+ and Cl- transport pathways of lamprey (Lampetra fluviatilis) erythrocytes was studied. In isosmotic medium, unidirectional K+ and Cl- effluxes appear to be largely mediated by conductive pathways. Unidirectional Cl- efflux increased as a function of a decrease in medium osmolarity. The swelling-activated Cl- transport was inhibited by R(+)-[(2-n-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo- 1H-inden-5-yl)oxy]acetic acid (DIOA), furosemide, and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In contrast, moderate cell swelling did not increase unidirectional ouabain-insensitive K+ efflux. However, inhibition of transport by Ba2+ was markedly reduced. This suggests that the Ba2+-sensitive pathway that mediated most of the K+ efflux in isosmotic conditions was inhibited by cell swelling and a Ba2+-insensitive pathway was activated. DIOA had no effect on K+ efflux in isosmotic or hyposmotic medium. These data and the finding that substitution of NO3- or SCN- for Cl- had only a minor effect on the swelling-induced net extrusion of K+ and water indicate that the pathways for K+ and Cl-, activated by cell swelling, are conductive.
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