AJP - Gastrointestinal and Liver Physiology, Vol 258, Issue 3 419-G425, Copyright © 1990 by American Physiological Society
Exocrine secretion and processing of pro-xenopsin in rat gastric lumen
C. F. Ferris, K. Muraki and R. E. Carraway
Department of Physiology, University of Massachusetts Medical Center, Worcester 01655.
This study examines the effects of acid, acid secretagogues, and pepstatin
on gastric luminal concentrations of xenopsin-like immunoreactivity (XPLI)
by in situ luminal perfusion of the stomach in anesthetized rats. During
perfusion with saline over a 2-h period, the concentration of XPLI fell in
parallel with acid output. Levels of XPLI fell more rapidly when the saline
contained 20 micrograms/ml pepstatin A and when phosphate-buffered saline
(pH 7.0) was used. These treatments did not, however, alter acid output.
After a basal condition was established at 90 min, intravenous injection of
carbachol, pentagastrin, or histamine stimulated acid and pepsin secretion
and also led to an increase in XPLI concentration, which was pepstatin
sensitive. Acid itself was also a stimulus for pepsin and XPLI output,
which were correlated at various levels of acidity. Although pepstatin
blocked the effect of acid on XPLI output, it did not lead to an
accumulation of xenopsin (XP) precursor in the luminal fluid. However, the
decrement in acid-stimulated XPLI output seen in the presence of pepstatin
was matched by an increment in XP precursor associated with the mucosal
surface. During high-pressure liquid chromatography, approximately 70% of
the acid-generated XPLI eluted at the position of mammalian XP. These data
support the notion that, during heightened acid output, XP is secreted by a
pepsin-dependent process or generated by the action of pepsin on XP
precursor present on the mucosal surface of the rat stomach.
