Abstract
Neuropeptide Y (NPY) has been shown to increase basal gastric acid secretion in dogs. We examined the hypothesis that NPY might increase gastric acid secretion by interaction with central catecholaminergic control of acid secretion in dogs. Studies were performed in awake canines with gastric fistulas and cerebroventricular guides which allowed injection into the lateral cerebral ventricle. Intracerebroventricular (i.c.v.) injection of yohimbine (5 μg/kg) increased acid secretion compared to control (yohimbine: 9.1 ± 3.3mmol//h;control: 1.8 ± 1.0mmol/2h, P < 0.05), whereas prazosin and propranolol (both 5 μg/kg i.c.v.) had no effect, suggesting that there is tonic central α 2-adrenergic inhibition of acid secretion. NPY 13–36 significantly increased acid secretion compared to control (NPY 13–36 1000pmol/kg i.c.v.: 5.6 ± 1.9mmol/2h;control: 1.3 ± 0.8mmol/2h, P < 0.05), whereas [Leu 31, Pro 34]-NPY had no effect, suggesting that the central effect of NPY is mediated at a Y 2, probably pre-synaptic receptor. Finally, i.c.v. desmethylimipramine (DMI) inhibited the acid response to i.c.v. NPY when injected before but not after NPY (i.c.v. DMI then i.c.v. NPY: control,15.2 ± 6.6mmol/2h;DMI, 3.5 ± 1.2mmol/2h, P< 0.05; i.c.v. NPY followed by i.c.v. DMI: control,8.9 ± 4.0mmol/2h;DMI, 9.9 ± 2.9mmol/2h, P > 0.05). This suggests that NPY acts by decreasing noradrenaline release. These findings are compatible with the hypothesis that i.c.v. NPY increases acid secretion by decreasing tonic central adrenergic inhibition of acid by decreasing release of noradrenaline at pre-synaptic level.
Published Version
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