AJP - Gastrointestinal and Liver Physiology, Vol 254, Issue 2 201-G209, Copyright © 1988 by American Physiological Society
Somatostatin modulates cholinergic neurotransmission in canine antral muscle
C. B. Koelbel, G. van Deventer, S. Khawaja, M. Mogard, J. H. Walsh and E. A. Mayer
Center for Ulcer Research and Education, Veterans Administration, Los Angeles, California.
Somatostatin has been shown to inhibit antral motility in vivo. To examine
the effect of somatostatin on cholinergic neurotransmission in the canine
antrum, we studied the mechanical response of and the release of
[3H]acetylcholine from canine longitudinal antral muscle in response to
substance P, gastrin 17, and electrical stimulation. In unstimulated
tissues, somatostatin had a positive inotropic effect on spontaneous phasic
contractions. In tissues stimulated with substance P and gastrin 17, but
not with electrical stimulation, somatostatin inhibited the phasic
inotropic response dose dependently. This inhibitory effect was abolished
by indomethacin. Somatostatin stimulated the release of prostaglandin E2
radioimmunoreactivity, and prostaglandin E2 inhibited the release of
[3H]acetylcholine induced by substance P and electrical stimulation.
Somatostatin increased the release of [3H]acetylcholine from unstimulated
tissues by a tetrodotoxin-sensitive mechanism but inhibited the release
induced by substance P and electrical stimulation. These results suggest
that somatostatin has a dual modulatory effect on cholinergic
neurotransmission in canine longitudinal antral muscle. This effect is
excitatory in unstimulated tissues and inhibitory in stimulated tissues.
The inhibitory effect is partially mediated by prostaglandins.
