Haemodynamic and Exocrine Effects of Caerulein at Submaximal and Supramaximal Levels on the Rat Pancreas: Role of Cholecystokinin Receptor Subtypes
| Autor: | Thomas Griesbacher, Irmgard Rainer, Akos Heinemann, Diana Groisman |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Agonist
medicine.medical_specialty Indoles medicine.drug_class Stimulation digestive system Cholecystokinin receptor Rats Sprague-Dawley Internal medicine Bradykinin B2 Receptor Antagonists Gastrins Animals Medicine Receptor General Environmental Science Cholecystokinin business.industry digestive oral and skin physiology Antagonist medicine.disease Pancreas Exocrine Receptor Cholecystokinin B Stimulation Chemical Rats Receptor Cholecystokinin A Endocrinology Pancreatitis Regional Blood Flow Cholecystokinin B receptor General Earth and Planetary Sciences Female Receptors Cholecystokinin business Ceruletide hormones hormone substitutes and hormone antagonists |
| Zdroj: | Pancreatology. 6:65-76 |
| ISSN: | 1424-3903 |
| Popis: | Background: We have investigated the involvement of cholecystokinin (CCK) receptor subtypes in haemodynamic changes in the pancreas of anaesthetized rats during submaximal and supramaximal stimulation with the CCK analogue, caerulein. Methods: For submaximal stimulation, caerulein (0.4 nmol/kg/h) was infused intravenously, while acute pancreatitis was induced by intraperitoneal injections of high doses of caerulein (3 × 25 nmol/kg). Pancreatic blood flow was measured by hydrogen clearance. Results: Low caerulein doses increased pancreatic blood flow by 26 ± 8% and vascular conductance by 24 ± 4%. This effect was mimicked by the CCK2 agonist gastrin-17. All effects were abolished by a CCK2 antagonist while a CCK1 antagonist remained inactive. Conversely, amylase output by caerulein was abolished by CCK1 receptor blockade, but not by inhibition of CCK2 receptors. During caerulein-induced pancreatitis, vascular conductance increased by 109 ± 26% and remained elevated throughout the experiment; vascular flow initially increased by 62 ± 27% and then returned to baseline. The vascular effects were prevented by a CCK2 receptor antagonist, while the induction of pancreatitis was due to CCK1 receptor stimulation. Conclusions: Caerulein increases pancreatic vascular flow via activation of CCK2 receptors. This effect occurs both at submaximal and at supramaximal levels of exocrine stimulation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect