Role of adrenoceptors and dopamine D2 receptors in the effects of bromocriptine on histamine -induced gastric acid secretion in male rat

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. 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. 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. It is possible that effect of bromocriptine on histamine-stimulated gastric acid secretion does not mediated via D2 dopaminergic and β adrenergic receptors