Peripheral bombesin induces gastric vagal afferent activation in
rats.
Yoshida-Yoneda, Eriko, Tj O-Lee, Jen Yu Wei, Steven R. Vigna, and
Yvette Tach[acute]e.
CURE/Digestive Disease Research Center, West Los Angeles VA Medical
Center, Dept of Medicine and Brain Research Institute, UCLA, Los
Angeles, CA 90073 and Department of Cell Biology, Duke University
Medical Center, Durham, NC 27710
APStracts 3:0244R, 1996.
Bombesin influence on gastric vagal afferent discharge (GVAD) was
studied in urethane-anesthetized rats. Vehicle and peptides were
injected iv at 30 min intervals. CCK (300 pmol) and bombesin (300
pmol) increased on-going multi-unit GVAD by 153 +/- 59% and 162 +/-
37% respectively; similar increases were induced by a second
injection of bombesin and CCK. The bombesin antagonist, ICI-216140
prevented bombesin-induced increase in GVAD while the CCK response
was not influenced. The CCK-A receptor antagonist, devazepide,
reduced the activation of GVAD induced by bombesin from 107 +/- 11%
to 63 +/- 6%, while abolishing the CCK response. Devazepide given
alone or in combination with ICI-216140 did not modify gastric
distension (3-ml) induced increase in GVAD. Of 22 single-units that
were activated by gastric load (4 ml), 17 and 20 units responded also
to bombesin (620 pmol) and CCK (870 pmol) respectively. Of the 9
units which did not respond to gastric load, 8 had an increase in
GVAD induced by both bombesin and CCK. There was no specific binding
of 125I-[Tyr4]-bombesin on cervical vagus either intact or 24 h after
ligation. These data suggest that iv bombesin-induced stimulation of
GVAD is indirect and initially mediated through specific receptor
activation influencing gastric smooth muscle and the release of CCK.
Received 21 December 1995; accepted in final form 14 June 1996.
APS Manuscript Number R807-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96