AJP - Gastrointestinal and Liver Physiology, Vol 249, Issue 2 284-G293, Copyright © 1985 by American Physiological Society
Ion transport in goby intestine: cellular mechanism of urotensin II stimulation
C. A. Loretz, M. E. Howard and A. J. Siegel
The Na- and Cl-absorbing goby posterior intestinal epithelium is composed
predominantly of mitochondria-rich, tall columnar cells. Glass
intracellular microelectrode recording technique was applied to absorptive
cells of this relatively leaky epithelium to measure apical cell membrane
potential difference (psi mc) and apical membrane fractional resistance. As
determined by ion-substitution studies, absorptive cells are characterized
by a large, Ba2+-inhibitable apical K conductance, which is a major factor
determining psi mc and smaller Cl and Na conductances. Inhibition of the
apical Na-Cl-coupled influx directly by furosemide or indirectly by the
phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine produced
hyperpolarization of psi mc, consistent with the greater apical membrane
conductance to Cl than Na. The urophysial neurosecretory peptide urotensin
II, which stimulates Na-Cl-coupled absorption, markedly depolarized psi mc
in posterior intestinal tissues from 5% seawater-adapted gobies. This
response is consistent with a stimulatory effect of urotensin II at the
apical membrane carrier rather than at the basolateral Na-K-ATPase.
Urotensin II is without effect on psi mc in tissues from seawater-adapted
fish and somatostatin, a natural analogue of urotensin II, is without
effect on tissues from fish adapted to either salinity. This specificity
parallels that determined using radiotracer fluxes.
