Humphreys G A, Davison J S, Veale W L
Department of Medical Physiology, Faculty of Medicine, University of Calgary, Alberta, Canada.
Am J Physiol. 1992 Nov;263(5 Pt 1):G726-32. doi: 10.1152/ajpgi.1992.263.5.G726.
Injection of neuropeptide Y (NPY) into the hypothalamic paraventricular nucleus (PVN) inhibits gastric acid secretion in anesthetized rats. The role of the autonomic nervous system in mediation of this response was investigated. Unilateral microinjection of 200 pmol NPY into the PVN of anesthetized rats inhibited spontaneous and pentagastrin-stimulated gastric acid output. Inhibition was abolished by subdiaphragmatic vagotomy, atropine, and bethanechol but was restored by electrical stimulation of the distal cut end of the vagus in cervically vagotomized rats. Although sympathectomy, phenoxybenzamine, and yohimbine abolished the inhibition, it was not affected by prazosin treatment. Gastric blood flow was not altered by injection of NPY. These results suggest that the antisecretory effect of NPY in the PVN was sympathetically mediated via suppression of gastric vagal cholinergic tone through activation of alpha 2-adrenoceptors.
向麻醉大鼠的下丘脑室旁核(PVN)注射神经肽Y(NPY)可抑制胃酸分泌。研究了自主神经系统在介导该反应中的作用。向麻醉大鼠的PVN单侧微量注射200 pmol NPY可抑制自发和五肽胃泌素刺激的胃酸分泌。膈下迷走神经切断术、阿托品和氨甲酰甲胆碱可消除这种抑制作用,但在颈部迷走神经切断的大鼠中,通过电刺激迷走神经的远端切断端可恢复抑制作用。虽然交感神经切除术、酚苄明和育亨宾可消除这种抑制作用,但哌唑嗪治疗对其无影响。注射NPY不会改变胃血流量。这些结果表明,PVN中NPY的抗分泌作用是通过激活α2-肾上腺素能受体,抑制胃迷走神经胆碱能张力,由交感神经介导的。