Concerted actions of il-1[beta] inhibit na+ absorption and
stimulate anion secretion by imcd cells.
Husted, Russell F., Chong Zhang, and John B. Stokes.
Laboratory of Epithelial Transport, Department of Internal
Medicine, University of Iowa and Department of Veterans Affairs
Medical Center, Iowa City, IA 52242
APStracts 5:0159F, 1998.
Increasing evidence indicates that factors other than adrenocorticoid
hormones can influence long term regulation of Na+ transport by inner
medullary collecting duct (IMCD) cells. We now report that of 14
interleukins tested, only IL-1[alpha] and IL-1[beta] inhibited Na+
transport by primary cultures of rat IMCD. IL-1[beta] reduced both
basal and mineralocorticoid (MC)-stimulated Na+ transport by 50-70%;
its effect on glucocorticoid (GC)-stimulated Na+ transport was
significantly less. IL-1[beta] continued to blunt MC stimulation of
Na+ transport even after it had been removed from the medium for 24
h. The onset of action to inhibit Na+ transport was within 20
minutes. The acute effect from the basolateral surface was greater
than the apical surface but the effect from each surface was
additive. In addition to its inhibitory effect on Na+ transport,
chronic IL-1[beta] exposure increased both basal and cAMP-stimulated
anion secretion rates. IL-1[beta] had no acute effect on anion
secretion. Monolayers chronically treated with IL-1[beta] had an
increased capacity to secrete fluid, as predicted from its effects on
ion transport. Inhibitors of cyclooxygenase did not blunt the actions
of IL-1[beta]. Furthermore, IL-1[beta] did not produce a rise in
intracellular Ca2+. These results suggest novel signaling pathways
induced by IL-1[beta] regulating Na+ and Cl- transport by the IMCD.
Received 7 May 1998; accepted in final form 3 September 1998.
APS Manuscript Number F110-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 21 September 1998