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Somatostatin modulates cholinergic neurotransmission in canine antral muscle

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:6945654
; ; ; ; ;  [1]
  1. Wadsworth Hospital, Los Angles, CA (USA) UCLA Medical Center, Torrance, CA (USA)
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 ({sup 3}H)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 E{sub 2} radioimmunoreactivity, and prostaglandin E{sub 2} inhibited the release of ({sup 3}H)acetylcholine induced by substance P and electrical stimulation. Somatostatin increased the release of ({sup 3}H)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 neutrotransmission 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.
OSTI ID:
6945654
Journal Information:
American Journal of Physiology; (USA), Journal Name: American Journal of Physiology; (USA) Vol. 254:2; ISSN 0002-9513; ISSN AJPHA
Country of Publication:
United States
Language:
English

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