Prostaglandin E2 induced the cyclic AMP-dependent release of acetylcholine in circular muscles of the isolated guinea pig ileum

1987 ◽  
Vol 83 (3) ◽  
pp. 293-297 ◽  
Author(s):  
J.T. Cheng ◽  
K. Shinozuka
2001 ◽  
Vol 132 (5) ◽  
pp. 999-1008 ◽  
Author(s):  
Stéphane Pelletier ◽  
Jean Dubé ◽  
Annie Villeneuve ◽  
Fernand Gobeil ◽  
Quan Yang ◽  
...  

1984 ◽  
Vol 246 (5) ◽  
pp. G509-G514 ◽  
Author(s):  
D. H. Teitelbaum ◽  
T. M. O'Dorisio ◽  
W. E. Perkins ◽  
T. S. Gaginella

The peptides caerulein, neurotensin, somatostatin, and substance P modulate the activity of intestinal neurons and alter gut motility. We examined the effects of these peptides on acetylcholine release from the myenteric plexus and intestinal contractility in vitro. Caerulein (1 X 10(-9) M), neurotensin (1.5 X 10(-6) M), and substance P (1 X 10(-7) M) significantly enhanced the release of [3H]acetylcholine from the myenteric plexus of the guinea pig ileum. This effect was inhibited by tetrodotoxin (1.6 X 10(-6) M). Somatostatin (10(-6) M) inhibited caerulein- and neurotensin-evoked release of acetylcholine but did not inhibit release induced by substance P. Caerulein, neurotensin, and substance P caused contraction of the guinea pig ileal longitudinal muscle. Somatostatin inhibited the contractions induced by caerulein and neurotensin. In contrast, substance P-induced contraction was not inhibited significantly by somatostatin. Thus, in the guinea pig ileum, caerulein-, neurotensin-, and substance P-induced contractility is due, at least in part, to acetylcholine release from the myenteric plexus. The ability of somatostatin to inhibit peptide-induced contractility is selective, and its mechanism may be attributed to inhibition of acetylcholine release.


1982 ◽  
Vol 32 (5) ◽  
pp. 938-940 ◽  
Author(s):  
Osamu YAGASAKI ◽  
Nobutaka SASAKI ◽  
Iwao YANAGIYA

1997 ◽  
Vol 66 (3) ◽  
pp. 131-137 ◽  
Author(s):  
J.A.J.M Dekkers ◽  
A.B.A Kroese ◽  
C.M Keenan ◽  
W.K MacNaughton ◽  
K.A Sharkey

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