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Histamine release in the isolated vascularly perfused stomach of the rat: regulation by autoreceptors
Author(s) -
Sandvik Arne K.,
Lewin Miguel J.M.,
Waldum Helge L.
Publication year - 1989
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.1476-5381.1989.tb11853.x
Subject(s) - histamine , medicine , gastrin , endocrinology , agonist , gastric acid , biology , basal (medicine) , pentagastrin , chemistry , receptor , secretion , insulin
1 In the isolated vascularly‐perfused stomach of the rat, gastrin 1–17 (520 pmol l −1 ) increased acid output from basal values of 13.7 ± 2.7 to 92.5 ± 11.4 μmol h −1 and venous histamine output from 10.1 ± 2.3 to 54.7 ± 7.9 nmol h −1 (mean ± s.e.mean). 2 The H 1 receptor agonist 2‐methylhistamine (10 μmol l −1 ) increased acid output to 21.6 ± 2.9 μmol h −1 ( P < 0.05) and reduced basal histamine output to 4.0 ± 0.8 nmol h −1 ( P < 0.05). Gastrin‐stimulated acid secretion and vascular histamine output was not significantly affected by 2‐methylhistamine (10 μmol l −1 ). 3 The H 2 receptor agonist, impromidine, dose‐dependently increased basal acid secretion, reaching a maximal value of 145.5 ± 11.7 μmol h −1 with impromidine (10 μmol l −1 ), and maximal gastrin‐stimulated acid secretion to 167.4 ± 15.1 μmol h −1 with impromidine (10 μmol l −1 ). Impromidine dose‐dependently inhibited basal and gastrin‐stimulated vascular histamine output. 4 The H 3 receptor agonist R‐a‐methylhistamine, (1 and 10 μmol l −1 ) minimally increased basal acid secretion. R‐a‐methylhistamine (10 μmol l −1 ) did not significantly affect maximal gastrinstimulated acid secretion. Basal and gastrin‐stimulated vascular histamine outputs decreased to 4.0 ± 0.8 ( P < 0.05) and 24.7 ± 4.7 nmol h −1 ( P = 0.05) with R‐a‐methylhistamine (10 μmol 1 −1 ). 5 The H 2 receptor antagonist ranitidine (2 μmol l −1 ) did not inhibit basal acid secretion, but acid outputs with gastrin and all histamine agonists were reduced. Ranitidine did not affect histamine release in the basal state, with gastrin or with any histamine agonist tested. 6 We conclude that gastric histamine release in the rat is regulated via a histamine H 2 receptor sensitive to the histamine agonists tested, but not to ranitidine. It is unlikely that the inhibition of histamine release is secondary to increased gastric acidity.