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STIMULATORY AND INHIBITORY HISTAMINE RECEPTORS IN CANINE CYSTIC DUCT
Author(s) -
CLANACHAN A.S.,
COURTNEY D.R,
SCOTT G.W.
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb09351.x
Subject(s) - cimetidine , histamine , endocrinology , medicine , histamine h1 receptor , agonist , cystic duct , diphenhydramine , chemistry , pharmacology , gallbladder , receptor , antagonist
1 The effects of histamine receptor stimulation were assessed on the resistance of the canine cystic duct in vivo and on the contractility of circular muscle preparations of canine cystic duct in vitro.2 In anaesthetized dogs, the H 1 ‐receptor agonist, 2‐pyridylethylamine (0.05 to 15 μmol, i.a.), elicited dose‐dependent increases in cystic duct resistance, whereas the H 2 ‐receptor agonist, 4‐methylhistamine (0.05 to 15 μmol, i.a.) decreased cystic duct resistance. These responses were antagonized by the H 1 ‐receptor antagonist, diphenhydramine, and the H 2 ‐receptor antagonist, cimetidine, respectively. 3 Histamine (0.1 to 3000 nmol, i.a.) also increased cystic duct resistance in vivo. In the presence of diphenhydramine, the stimulatory effect of histamine was antagonized and slight decreases in cystic duct resistance became apparent. Cimetidine or prazosin also antagonized the stimulatory effects of histamine. 4 Histamine (1 to 100 μ m ) or 2‐pyridylethylamine (1 to 100 μ m ) contracted, whereas 4‐methylhistamine (1 to 100 μ m ) relaxed, circular muscle preparations of cystic duct. These excitatory and inhibitory responses were antagonized by diphenhydramine and cimetidine, respectively. 5 These results indicate that the canine cystic duct possesses excitatory H 1 ‐ and inhibitory H 2 ‐receptors. The predominant effect of histamine is an H 1 ‐receptor‐mediated increase in cystic duct resistance. Histamine, which may be released in association with cholecystitis, may exert significant effects on the regulation of bile flow in and out of the gallbladder and may contribute to gallbladder stasis during biliary disease.