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Activation of histamine H3 receptors inhibits acetylcholine release from the rat stomach in vitro

The isolated rat stomach was vascularly perfused with modified Krebs-Ringer solution containing 100 microM physostigmine. Endogenous acetylcholine (ACh) released from the stomach was measured by enzyme reaction and electrochemical systems using HPLC. Electrical stimulation of bilateral vagus nerves...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1999, Vol.79 (suppl.1), p.82-82
Main Authors: Yokotani, Kunihiko, Nakamura, Kumiko, Osumi, Yoshitsugu
Format: Article
Language:English
Online Access:Get full text
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Summary:The isolated rat stomach was vascularly perfused with modified Krebs-Ringer solution containing 100 microM physostigmine. Endogenous acetylcholine (ACh) released from the stomach was measured by enzyme reaction and electrochemical systems using HPLC. Electrical stimulation of bilateral vagus nerves (0.5-2.0 Hz, 10 mA, 2 msec duration, for 2 min) evoked the release of ACh. This evoked release at 2.5 Hz was slightly potentiated by thioperamide (H3 antagonist). The evoked release of ACh at 0.5 Hz in the presence of atropine (10^-6 M) was inhibited by R-alpha-methylhistamine and imetit (H3 agonists) in a dose-dependent mannar (10^-8 -10^-5 M). The inhibition by R-alpha-methyl-histamine (10^-5 M) was abolished by thioperamide (10^-5 M) and that by imetit (10^-5 M) was abolished by pertusis toxin (10 microgram per rat, i.v., 4 days before experiment). On the other hand, amthamine (H2 agonist) (10^-7 -10^-5 M) had no effect on the evoked release of ACh. These results suggest that histamine attenuates the release of ACh from vagus nerve by H3 receptors and pertusis toxin-sensitive mechanisms in the stomach.
ISSN:0021-5198
1347-3506
DOI:10.1016/S0021-5198(19)34350-1