Hypotonicity induced K+ and anion conductive pathways activation in eel intestinal epithelium
2005
SUMMARY Control of cell volume is a fundamental and highly conserved physiological
mechanism, essential for survival under varying environmental and metabolic
conditions. Epithelia (such as intestine, renal tubule, gallbladder and gills)
are tissues physiologically exposed to osmotic stress. Therefore, the
activation of `emergency9 systems of rapid cell volume regulation is
fundamental in their physiology. The aim of the present work was to study the
physiological response to hypotonic stress in a salt-transporting epithelium,
the intestine of the euryhaline teleost Anguilla anguilla . Eel
intestinal epithelium, when symmetrically bathed with Ringer solution,
develops a net Cl - current giving rise to a negative
transepithelial potential at the basolateral side of the epithelium. The eel intestinal epithelium responded to a hypotonic challenge with a
biphasic decrease in the transepithelial voltage ( V te ) and
the short circuit current ( I sc ). This electrophysiological
response correlated with a regulatory volume decrease (RVD) response, recorded
by morphometrical measurement of the epithelium height. Changes in the
transepithelial resistance were also observed following the hypotonicity
exposure. The electrogenic V te and I sc
responses to hypotonicity resulted from the activation of different
K + and anion conductive pathways on the apical and basolateral
membranes of the epithelium: (a) iberiotoxin-sensitive K + channels
on the apical and basolateral membrane, (b) apamin-sensitive K +
channels mainly on the basolateral membrane, (c) DIDS-sensitive anion channels
on the apical membrane. The functional integrity of the basal Cl -
conductive pathway on the basolateral membrane is also required. The electrophysiological response to hypotonic stress was completely
abolished by Ca 2+ removal from the Ringer perfusing solution, but
was not affected by depletion of intracellular Ca 2+ stores by
thapsigargin.
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