جستجوی مقالات مرتبط با کلیدواژه "d2 receptors" در نشریات گروه "پزشکی"

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

Several studies indicate that central serotonergic neurons have important role in morphine analgesia and tolerance.The aim of this study was to investigate possible role of 5-HT1A receptors by chronic administration of buspirone (partial agonist of 5- HT1A receptors) in producing analgesic effect and on development of tolerance to analgesic effect of morphine using hot plate test. Experiments were performed on adult male mice weighing between 20 and 25 g. The control mice (n=8) had daily i.p. injection of morphine (5mg/kg/day). In the vehicle and test groups before injection of morphine (5mg/kg/day, i.p.), we injected vehicle of buspirone (saline normal: 0.5 ml/kg/day, i.p.) and buspirone (5, 7.5 and 10 mg/kg/day, i.p.) respectively and the hot-plate test just before and 30 minutes after the morphine injection performed once every 5 days. Experiments were continued for 5 days after the attainment of tolerance to analgesic effect of morphine. In the another three groups, we injected only buspirone (5, 7.5 and 10 mg/kg/day, i.p.) and the hot-plate test just before and 30 minutes after the buspirone injection performed once every 5 days for the evaluation of the analgesic effect of buspirone in chronic uses. Chronic injection of buspirone (5, 7.5 and 10 mg/kg/day, i.p.) significantly delayed tolerance to morphine analgesia (p<0.05). In addition, chronic administration of buspirone (5, 7.5 and 10 mg/kg/day, i.p.) produce significant analgesic effect (p<0.05). The results confirmed the important role of 5-HT1A receptors in analgesia and the development of tolerance to morphine and may dissolve clinical problems due to long duration of opioides administration. However, the exact mechanism of interaction between serotonergic and opioidergic systems is not clear and remains to be elucidated.