CCK-evoked hyperemia in rat gastric mucosa involves neural mechanisms and nitric oxide
| Autor: | Peter Holzer, Brigitta M. Peskar, M. Jocic, Akos Heinemann |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
Physiology Calcitonin Gene-Related Peptide Hyperemia Vagotomy Calcitonin gene-related peptide Nitric Oxide Sincalide Nitric oxide Gastric Acid Rats Sprague-Dawley chemistry.chemical_compound Physiology (medical) Internal medicine medicine Gastric mucosa Animals Nervous System Physiological Phenomena Cholecystokinin Hepatology Vagovagal reflex Stomach digestive oral and skin physiology Gastroenterology Peptide Fragments Rats NG-Nitroarginine Methyl Ester medicine.anatomical_structure Endocrinology chemistry Gastric Mucosa Regional Blood Flow Capsaicin Gastric acid Female |
| Zdroj: | Europe PubMed Central |
| ISSN: | 1522-1547 0193-1857 |
| DOI: | 10.1152/ajpgi.1996.270.2.g253 |
| Popis: | This study was performed to identify the possible neural mechanisms and mediators that underlie the gastric mucosal hyperemia evoked by cholecystokinin octapeptide (CCK-8). Gastric mucosal blood flow in anesthetized rats was assessed by the clearance of hydrogen and gastric acid secretion determined in the luminally perfused stomach. The gastric mucosal hyperemic effect of a low dose of CCK-8 (0.04 nmol/min iv infusion for 7 min) was abolished by inhibition of nitric oxide synthesis with NG-nitro-L-arginine methyl ester (15 mg/kg iv) and significantly blunted by defunctionalization of afferent neurons with a neurotoxic dose of capsaicin (125 mg/kg sc). The hyperemic reaction to a high dose of CCK-8 (0.2 nmol/min) was not significantly affected by these pharmacological maneuvers. The vasodilator response to low-dose CCK-8 (0.04 nmol/min) was further analyzed and found to be inhibited by acute bilateral subdiaphragmatic vagotomy, atropine (1 mumol/kg ip), and the antagonistic calcitonin gene-related peptide (CGRP) fragment CGRP-(8-37) (6 nmol/ min ia). Cyclooxygenase inhibition with indomethacin (10 mg/kg ip) was ineffective. The CCK-8-induced increment of gastric acid secretion was not significantly altered by any of these procedures. These results indicate that the gastric vasodilator effect of submaximal doses of CCK-8 is brought about by a vagovagal reflex that involves acetylcholine, CGRP or a related peptide, and nitric oxide as vasodilator messengers. |
| Databáze: | OpenAIRE |
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