Role of adrenoceptors and dopamine D2 receptors in the effects of bromocriptine on histamine -induced gastric acid secretion in male rat
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Date
2024-07-13
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Brieflands
Abstract
Introduction: Gastric acid secretion is one of the most
important causes of peptic ulcer. Dopamine and its agonists have a protective
role in the stomach. In the present study the role of α1 and β adrenoceptors
and dopamine D2 receptors in the effects of bromocriptine on
histamine-induced gastric acid secretion were evaluated. Materials and Methods: 93 Male Wistar rats
weighing between 180-220 g were used. After the induction of anesthesia with
ketamine/xylazine, for histamine infusion and tracheostomy, jugular vein and
trachea were exposed respectively. For injecting physiologic saline and
removing gastric secretion a polyethylene tube and a cannula was inserted into
the stomach through esophagus and pyloroduodenal junction respectively. Every
10 minute 2 milliliter Physiologic saline was introduced and removed through esophagial and pyloro duodenal tube
respectively during 2 hour period of experiment. pH of removed solution was
detected, using 0.1 N NaOH was titrated and then acid content was reported as
µEq/10 minute. Results: Gastric acid secretion was increased
significantly 30 minute after histamine (0.8 mg/100g/h) infusion and remained
high throughout experimental period. Administration of bromocriptine as a
dopamine D2 receptor agonist (8 mg/kg) before histamine infusion
significantly decreased stimulated gastric acid secretion. Domperidone
(peripheral D2 receptor antagonist) and or propranolol (β
adrenoceptor antagonist) injection before bromocriptine prominently augmented
effect of bromocriptine on histamine-stimulated gastric acid secretion. Conclusion: It is possible that effect of
bromocriptine on histamine-stimulated gastric acid secretion does not mediated
via D2 dopaminergic and β adrenergic receptors