title: Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: dose-response results under non-stress conditions and immobilization stress.
abstract: In non-stressed rats and rats stressed by immobilization, gastric secretion (acid, pepsin), mucosal blood flow (MBF), stress ulcers as well as glucose, insulin, and glucagon in blood were studied during 8 h, with and without additional infusion of exogenous glucagon (0.2, 1.4, 9.8 micrograms/kg/h). Metabolic clearance of glucagon and the disappearance half-time of exogenous glucagon from blood do not differ during zero stress and stress, a fact that favors the assumption of hypersecretion of glucagon as the cause of stress hyperglucagonemia. During stress alone acid secretion (volume, acidity) and MBF are lower than during zero stress; pepsin remains unchanged. Under zero stress condition additionally administered glucagon inhibits pepsin and MBF, but not acid secretion, in a dose-dependent manner. The ulcer index increased without changing the severity of ulcers. During stress the intermediate and highest glucagon doses stimulate MBF and pepsin secretion, other variables remaining unchanged. It is concluded that glucagon effects on functions of the gastric mucosa in the rat vary fundamentally, depending upon the environmental conditions.
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000098:blood supply*; D005934:Glucagon / Q000008:administration & dosage / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow; D012149:Restraint, Physical; D013276:Stomach Ulcer / Q000209:etiology* / Q000378:metabolism; D013312:Stress, Physiological / Q000150:complications / Q000503:physiopathology*
chemical_list: D005934:Glucagon; D005947:Glucose