EFFECT OF ANGIOTENSIN ON THE RELEASE OF ACETYLCHOLINE FROM PREGANGLIONIC AND POSTGANGLIONIC NERVE ENDINGS

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.

1981 ◽  
Vol 59 (6) ◽  
pp. 541-547 ◽  
Author(s):  
John G. Clement

Early studies indicated that the BaCl2-induced contractions in the guinea pig ileum longitudinal muscle strip (GPI-LMS) were, in part, neuronal in origin. However, recent studies have suggested that BaCl2-induced contractions were produced by an action directly on the smooth muscle membrane. The purpose of this study was to investigate the mechanism of the BaCl2 contractions in the GPI-LMS. Botulinum toxin (5 × 105 MLD/mL), which blocks the electrically induced release of acetylcholine (ACh), hemicholinium-3 (HC-3; 110 μM), which blocks ACh synthesis, tetrodotoxin (TTX; 60 nM), which blocks Na+ channels, black widow spider venom, which depletes the presynaptic neuron of neurotransmitter, and atropine (2.9 μM), a potent muscarinic antagonist, had no effect on the BaCl2 contractions. Desensitization of the GPI-LMS to substance P did not affect the BaCl2 contraction. In Ca2+-free buffer the BaCl2 dose–response curve was shifted to the right. In Ca2+-free solution the time to 50% inhibition of the contractile response to ACh (73 nM) and BaCl2 (1.16 mM) was 3.7 and 125 min, respectively. The D 600 IC50 for ACh and BaCl2 contractions was 220 and 130 nM, respectively. In Ca2+-free buffer either EGTA (0.53 mM) or D 600 (1 μM) were potent inhibitors of BaCl2 contractions. These results suggest that in the GPI-LMS the BaCl2 response is not mediated by a release of ACh (or substance P) because inhibitors of ACh release, synthesis, and receptors do not affect the responses. Also, the BaCl2 contraction is not due to activation of Na+ channels because TTX is without effect. The BaCl2-induced contraction appears to be mainly due to the movement of membrane bound Ca2+ through D 600 sensitive Ca2+ channels with extracellular Ca2+ and possible passage of Ba2+ ions intracellularly playing relatively minor roles.


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.


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