Pepsinogen secretion in cholecystokinin-1 receptor-deficient rats
| Autor: | Hayato Nakamura, Makoto Otsuki, Kenji Kanagawa |
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| Rok vydání: | 2004 |
| Předmět: |
Agonist
Male medicine.medical_specialty Pepsinogen A Physiology medicine.drug_class Rats Inbred OLETF Stimulation Biology digestive system Cholecystokinin receptor Sensitivity and Specificity Sincalide Statistics Nonparametric Species Specificity Reference Values Risk Factors Internal medicine Gastrins medicine Animals Rats Long-Evans Receptor Cholecystokinin Probability digestive oral and skin physiology Gastroenterology Receptor antagonist digestive system diseases Rats Receptor Cholecystokinin A Disease Models Animal Somatostatin Endocrinology Receptors Cholecystokinin hormones hormone substitutes and hormone antagonists |
| Zdroj: | Digestive diseases and sciences. 49(9) |
| ISSN: | 0163-2116 |
| Popis: | We examined the roles of cholecystokinin (CCK)-2 receptors in the regulation of pepsinogen secretion in the CCK-1 receptor deficient Otsuka Long–Evans Tokushima Fatty (OLETF) rats. Pepsinogen secretion was determined in fasted acute fistula OLETF and control Long–Evans Tokusima Otsuka (LETO) rats. Pepsinogen secretion in OLETF rats under basal conditions as well as in response to CCK-8 stimulation was significantly higher than that in LETO rats. CCK-1 receptor specific agonist ARL 15849 was unable to stimulate pepsinogen secretion in OLETF rats, whereas it elicited pepsinogen secretion in LETO rats to levels similar to those obtained with equimolar CCK-8 stimulation. CCK-2 receptor antagonist reduced basal pepsinogen secretion and completely abolished CCK-8-stimulated pepsinogen output in OLETF rats, whereas in LETO rats, it reduced basal pepsinogen secretion but augmented CCK-8-stimulated pepsinogen output. CCK-1 receptor antagonist loxiglumide also greatly decreased CCK-8-stimulated pepsinogen secretion in OLETF rat, which indicates that loxiglumide is not a specific CCK-1 receptor antagonist. Intravenous infusion of somatostatin antagonist significantly increased CCK-8-stimulated pepsinogen secretion in LETO rats, whereas it had no significant influence on CCK-8-stimulated pepsinogen secretion in OLETF rats. These results indicate that CCK-8 stimulates pepsinogen secretion via CCK-2 receptors in CCK-1 receptor deficient OLETF rats and that the higher CCK-8-stimulated as well as basal pepsinogen secretion in OLETF rats might result from an elimination of tonic inhibition by somatostatin that is released from D cells through mainly CCK-1 receptors. |
| Databáze: | OpenAIRE |
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