包装 | 价格(元) |
1mg | 电议 |
5mg | 电议 |
10mg | 电议 |
Animal experiment: | Rats[1]The first set of experiments is carried out on rats with intact vagus nerves which are acutely treated with CCK-8S or Gastrin-1 at the doses of 1.5, 5, 15 and 45 nmol/kg. Both these peptides are administered i.v. as a bolus immediately after the collection of basal effluent samples. In experiments investigating the involvement of muscarinic, histamine H or CCK receptors in the gastric 2 secretory responses elicited by CCK-8S or Gastrin-1, the animals are pretreated with atropine 1 μmol/kg i.v., cimetidine 10 μmolrkg i.v., devazepide 1.25-2.5 μmol/kg i.v. or L-365,260 2.5-5 μmol/kg i.v., 10 min before ending the collection of the second basal effluent sample. Additional experiments are performed in animals pretreated with the irreversible inhibitor of histidine decarboxylase, α-fluoromethylhistidine (450 mmol/kg i.p. twice daily for two consecutive days), in order to suppress endogenous histamine production from digestive enterochromaffin-like cells[1]. |
产品描述 | Gastrin-1, human is the endogenous peptide produced in the stomach, and increases gastric acid secretion via cholecystokinin 2 (CCK2) receptor. Gastrin-1, human is the endogenous peptide produced in the stomach, and acts via cholecystokinin 2 (CCK2) receptor[1]. Gastrin-1 (1.5, 5, 15 and 45 nmol/kg, i.v.) increases pepsinogen and acid secretion in rats[1]. References: |