C. Duranton et al., Potassium channels in primary cultures of seawater fish gill cells. II. Channel activation by hypotonic shock, AM J P-REG, 279(5), 2000, pp. R1659-R1670
Citations number
35
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Previous studies performed on apical membranes of seawater fish gills in pr
imary culture have demonstrated the existence of stretch-activated K+ chann
els with a conductance of 122 pS. The present report examines the involveme
nt of K+ channels in ion transport mechanisms and cell swelling. In the who
le cell patch-clamp configuration, K+ currents were produced by exposing ce
lls to a hypotonic solution or to 1 muM ionomycin. These K+ currents were i
nhibited by the addition of quinidine and charybdotoxin to the bath solutio
n. Isotopic efflux measurements were performed on cells grown on permeable
supports using Rb-86(+) as a tracer to indicate potassium movements. Apical
and basolateral membrane Rb-86 effluxes were stimulated by the exposure of
cells to a hypotonic medium. During the hypotonic shock, the stimulation o
f Rb-86 efflux on the apical side of the monolayer was inhibited by 500 muM
quinidine or 100 muM gadolinium but was insensitive to scorpion venom [Lei
rus quinquestriatus hebraeus (LQH)]. An increased Rb-86 efflux across the b
asolateral membrane was also reduced by the addition of quinidine and LQH v
enom but was not modified by gadolinium. Moreover, basolateral and apical m
embrane Rb-86 effluxes were not modified by bumetanide or thapsigargin. The
re is convincing evidence for two different populations of K+ channels acti
vated by hypotonic shock. These populations can be separated according to t
heir cellular localization (apical or basolateral membrane) and as a functi
on of their kinetic behavior and pharmacology.