AJP - Cell Physiology, Vol 254, Issue 5 C643-C650, Copyright © 1988 by American Physiological Society
Potassium-induced cell swelling in Necturus gallbladder epithelium
C. W. Davis and A. L. Finn
Department of Physiology, University of North Carolina, School of Medicine, Chapel Hill 27599.
In Necturus gallbladder epithelium, elevation of mucosal K+ to 95 mM in the
presence of 10 mM Na+ resulted in cell swelling at a rate of 3.2% original
volume per minute, followed by volume-regulatory shrinking. When Na+ was
completely removed from or when amiloride (10(-4) M) was added to the
mucosal medium, K+-induced cell swelling was abolished. In the presence of
10 mM Na+, 1 mM Ba2+ abolished and substitution of mucosal Cl- by NO-3 had
no effect on K+-induced swelling. Thus solute entry following elevation of
mucosal K+ is effected by separate K+ and Cl- pathways. Furthermore,
substitution of 95 mM K+ for Na+ in the mucosal bathing medium leads to the
development of a Cl- conductance in the basolateral membrane as long as
some Na+ remains in the medium. However, cell swelling induced by mucosal
dilution does not lead to the appearance of a Cl- conductance. Thus the
activation of this conductance requires both swelling and membrane
depolarization. These results show that 1) high mucosal K+ leads to cell
swelling due to the entry of Cl- along with K+ and the Cl- can enter across
either membrane, 2) the Cl- pathways require the presence of mucosal Na+,
and 3) cell volume regulation is activated by an increase in volume per se,
i.e., a hyposmotic exposure is not required for volume regulation to occur.
