Article date: January 1991
By: S. Evangelista, C.A. Maggi, in Volume 102, Issue 1, pages 119-122
We have investigated the effect of intravenous injection of cholecystokinin‐8 (CCK‐8) and other peptides on gastric lesion formation in response to an intragastric perfusion with 25% ethanol in rats anaesthetized with urethane.
Intravenous injection of CCK‐8 (50–100 nmol kg−1), but not bombesin (1–100 nmol kg−1), calcitonin gene‐related peptide (1–50 nmol kg−1), neurokinin A (1 μmol kg−1) or substance P (100 nmol kg−1), induced protection against gastric haemorrhagic lesions produced by ethanol.
The CCKA‐antagonist L‐364,718 (2.45 μmol kg−1, i.v.) increased the lesion index induced by ethanol and reversed the protective effect of CCK‐8 (50 nmol kg−1, i.v.). The CCKB‐antagonist L‐365,260 (5 μmol kg−1, i.v.) and a lower dose of L‐364,718 (0.25 μmol kg−1, i.v.) were ineffective.
The gastric protective effects afforded by CCK‐8 (50 nmol kg−1, i.v.) were not observed in vagotomized‐rats and were reduced by capsaicin pretreatment. In capsaicin‐pretreated rats there was a worsening of gastric lesions induced by ethanol‐perfusion as compared to those observed in vehicle‐pretreated rats.
These results demonstrate that the mucosal protective effect of CCK‐8 involves, at least in part, the activation of CCKA‐receptors and is mediated by vagal capsaicin‐sensitive fibres.
We have investigated the effect of intravenous injection of cholecystokinin‐8 (CCK‐8) and other peptides on gastric lesion formation in response to an intragastric perfusion with 25% ethanol in rats anaesthetized with urethane.
Intravenous injection of CCK‐8 (50–100 nmol kg−1), but not bombesin (1–100 nmol kg−1), calcitonin gene‐related peptide (1–50 nmol kg−1), neurokinin A (1 μmol kg−1) or substance P (100 nmol kg−1), induced protection against gastric haemorrhagic lesions produced by ethanol.
The CCKA‐antagonist L‐364,718 (2.45 μmol kg−1, i.v.) increased the lesion index induced by ethanol and reversed the protective effect of CCK‐8 (50 nmol kg−1, i.v.). The CCKB‐antagonist L‐365,260 (5 μmol kg−1, i.v.) and a lower dose of L‐364,718 (0.25 μmol kg−1, i.v.) were ineffective.
The gastric protective effects afforded by CCK‐8 (50 nmol kg−1, i.v.) were not observed in vagotomized‐rats and were reduced by capsaicin pretreatment. In capsaicin‐pretreated rats there was a worsening of gastric lesions induced by ethanol‐perfusion as compared to those observed in vehicle‐pretreated rats.
These results demonstrate that the mucosal protective effect of CCK‐8 involves, at least in part, the activation of CCKA‐receptors and is mediated by vagal capsaicin‐sensitive fibres.
DOI: 10.1111/j.1476-5381.1991.tb12142.x
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