Somatostatin excites canine ileum ex vivo: role for no?. P., Vergara, Woskowska Z., Cipris S., Fox-Threlkeld J. E. T. and E. E. Daniel. Division of Physiology and Pharmacology, McMaster University, 1200 Main Street West, Hamilton, Ontario L8N 3Z5
APStracts 2:0021G, 1995.
Isolated perfused segments of canine ileum have no spontaneous motor activity, and release large quantities of vasoactive intestinal polypeptide (VIP) continuously. Somatostatin perfusion was shown to decrease VIP release, accompanied by increased contractions and amplification of responses to low frequency electrical field stimulation. After perfusion of higher somatostatin concentrations, the VIP output did not recover but quiescence returned. The actions of somatostatin on motor activity were not modified by hexamethonium, slightly reduced by atropine and markedly reduced by tetrodotoxin (TTX). Inhibition of VIP output was not the major determinant of motor activity in the ileum because: 1) a second infusion of somatostatin had similar motor effects despite markedly reduced VIP output; 2) abolition of tonic VIP output did not prevent induction of motor activity by somatostatin; and 3) artificial restoration of VIP levels did not prevent or antagonize somatostatin induced ileal contractions. In contrast, the increment in motor responses induced by somatostatin was not apparent after L-N_-arginine methyl ester, an inhibitor of NO synthase, but recovered after reversal by L-arginine. We conclude that the mode of somatostatin activation of intestinal motor activity involves reduced nitric oxide output, enhanced excitatory mediator action or release, a direct action on smooth muscle and possibly inhibition of VIP output. Of these, reduced nitric oxide output plays the most important role.

Received 15 October 1993; accepted in final form 1 February 1995.
APS Manuscript Number G412-3.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.