scholarly journals THE EFFECTS OF INERT GASES AND OTHER GENERAL ANAESTHETICS ON THE RELEASE OF ACETYLCHOLINE FROM THE GUINEA-PIG ILEUM

1979 ◽  
Vol 67 (2) ◽  
pp. 229-237 ◽  
Author(s):  
D.J.X. HALLIDAY ◽  
HILARY J. LITTLE ◽  
W.D.M. PATON
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

1981 ◽  
Vol 59 (3) ◽  
pp. 307-310 ◽  
Author(s):  
K. Jhamandas ◽  
J. Elliott ◽  
M. Sutak

Eseroline, an eserine derivative without anticholinesterase activity, was tested in several systems for opiatelike activity. Eseroline depressed the twitch of the field-stimulated guinea pig ileum myenteric plexus longitudinal muscle preparation but failed to depress the twitch of the rat vas deferens. Intraperitoneal injections of eseroline in rats induced naloxone-antagonizable analgesia and catalepsy. Eseroline failed to influence the release of acetylcholine from the cortex of anesthetized rats. These observations have implications for studies in which eserine is used as a pharmacological tool.


1967 ◽  
Vol 45 (2) ◽  
pp. 313-317 ◽  
Author(s):  
J. -C. Panisset

Angiotensin is known to stimulate the synaptic transmission of the cat superior ganglion and the contraction of the isolated guinea pig ileum; to determine whether these effects could be mediated by a cholinergic mechanism, both preparations were tested for the possible release of acetylcholine by angiotensin. The right cervical ganglion of 12 anesthetized cats was perfused with heparinized cat plasma, and the preganglionic sympathetic trunk was electrically stimulated supramaximally at 10-min intervals. After each stimulation, the acetylcholine content of the effluent was determined by bioassay. Angiotensin, injected intraarterially toward the ganglion in amounts ranging from 0.1 to 100 ng immediately before a stimulation period induced a 30 to 50% increase in acetylcholine output. Most effective doses ranged from 0.5 to 20 ng. Comparable experiments were carried out on coaxially stimulated strips of guinea pig ileum in Krebs solution. The addition of angiotensin, 1 ng/ml, was followed by a 4.3-fold increase in acetylcholine release during the period of contractile stimulation. From these two sets of data, it is concluded that angiotensin exerts a cholinergic action at the preganglionic level in the ganglion and at a postganglionic site in the ileum.


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