Sites of actions of adenosine in intrinsic cholinergic nerves of ileal longitudinal muscle from guinea pig

It has been noted that the analgesic property of ethanol bears a marked resemblance to that of morphine. The purpose of this study was to determine if the mechanism of action of morphine and ethanol was similar using the guinea pig ileal longitudinal muscle strip (GPI-LMS). Ethanol (35–260 mM) depressed the twitch response and the acetylcholine- (ACh-), KCl-, and BaCl2-induced contractions to the same extent while having no significant effect on the binding of [3H]quinuclidinyl benzilate ([3H]QNB) to muscarinic receptors. Morphine (53–530 nM) inhibited the twitch response and to a lesser extent BaCl2- and KCl-induced contractions while having no significant effect on either ACh-induced contractions or the binding of [3H]QNB to muscarinic receptors. Naloxone and increased [Ca2+] reversed the inhibitory effects of morphine but not ethanol. Ethanol appears to inhibit a site after interaction of ACh with the receptor. Mechanism of inhibition of BaCl2 response is also different as naloxone and increased [Ca2+] reverse morphine but not ethanol inhibition. Ethanol inhibition in GPI-LMS does not involve the opiate receptor.

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EFFECT OF PROSTAGLANDIN K AND INDOMETHACIN ON RESPONSES OF LONGITUDINAL MUSCLE OF GUINEA-PIG ILEUM TO CHOLECYSTOKININ

Abstracts ◽

10.1016/b978-0-08-023768-8.51799-0 ◽

1978 ◽

pp. 686

Author(s):

J. Zséli ◽

E.S. Vizi ◽

J. Knoll

Keyword(s):

Guinea Pig ◽

Longitudinal Muscle ◽

Guinea Pig Ileum

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Somatostatin modulation of peptide-induced acetylcholine release in guinea pig ileum

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1984.246.5.g509 ◽

1984 ◽

Vol 246 (5) ◽

pp. G509-G514 ◽

Cited By ~ 5

Author(s):

D. H. Teitelbaum ◽

T. M. O'Dorisio ◽

W. E. Perkins ◽

T. S. Gaginella

Keyword(s):

Substance P ◽

Guinea Pig ◽

Myenteric Plexus ◽

Acetylcholine Release ◽

Longitudinal Muscle ◽

Guinea Pig Ileum ◽

Gut Motility ◽

Release Of Acetylcholine

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.

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Inhibitory effects of isoprenaline and calcium on contractions of guinea pig ileal longitudinal muscle

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)66635-7 ◽

1977 ◽

Vol 27 ◽

pp. 162

Author(s):

Yukio Ishida ◽

Nobuaki Kondo ◽

Kaoruko Fujii ◽

Yoshiko Sekimoto

Keyword(s):

Guinea Pig ◽

Longitudinal Muscle ◽

Inhibitory Effects

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Acetylcholine release from canine isolated airway is not modulated by norepinephrine

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.3.1025 ◽

1986 ◽

Vol 61 (3) ◽

pp. 1025-1030 ◽

Cited By ~ 18

Author(s):

J. G. Martin ◽

B. Collier

Keyword(s):

Guinea Pig ◽

Acetylcholine Release ◽

Electrical Field Stimulation ◽

Output Pulse ◽

Physiological Salt Solution ◽

Guinea Pig Ileum ◽

Cholinergic Nerves ◽

Ach Release ◽

Electrical Field ◽

Neural Origin

We measured acetylcholine (ACh) release from canine isolated tracheal smooth muscle (TSM) and bronchial spirals using a radioenzymic assay technique. Tissue was incubated in physiological salt solution containing physostigmine (3.10(-5) M), atropine (10(-7) M), and choline (5.10(-6) M), and bath fluid was collected every 15 min for assay. There was a resting release of ACh of 209 +/- 44 pmol/g tissue (mean +/- SE) from 53 to 77 specimens of TSM. Electrical field stimulation (ES) increased ACh release, which was blocked by tetrodotoxin (10(-6) g/ml), confirming the neural origin of ACh. The ACh output during ES (2-ms pulses) at 10 Hz increased linearly from 188 +/- 50 pmol/g tissue (mean +/- SE) for a 1-min volley, to 323 +/- 57 for three volleys, and 544 +/- 128 for five volleys. The ACh output/pulse was constant during ES at 20, 15, 10, and 5 Hz, but it was significantly higher at 2 than at 5 Hz (P less than 0.005). Incubation of TSM with norepinephrine (NE, 10(-5) M) did not affect ACh output either at 2 or 10 Hz. Likewise, ACh output from bronchial spirals during ES and 2 Hz was unaffected by NE. In contrast, NE treatment of isolated guinea pig ileum reduced the ACh released by ES at 2 Hz to 40 +/- 7% (P less than 0.001) of the control ACh output. It is concluded that evoked release of ACh (output/pulse) from cholinergic nerves in canine airway is frequency dependent, as in guinea pig ileum, but that, unlike guinea pig ileum, NE does not modulate its release.

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