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大鼠三叉神经旁核中缓激肽介导的升压效应。

Pressor effect mediated by bradykinin in the paratrigeminal nucleus of the rat.

作者信息

Lindsey C J, Buck H S, Fior-Chadi D R, Lapa R C

机构信息

Department of Biophysics, Escola Paylista de Medicina, Universidade Federal de São Paulo, Brazil.

出版信息

J Physiol. 1997 Jul 1;502 ( Pt 1)(Pt 1):119-29. doi: 10.1111/j.1469-7793.1997.119bl.x.

Abstract
  1. The participation of the paratrigeminal nucleus (Pa5) in the pressor response produced by bradykinin in the dorsolateral medulla of rats was investigated. The microinjection of 6 pmol of bradykinin directly over the paratrigeminal nucleus of unanaesthetized rats produced a significant increase in arterial pressure and a moderate increase in heart rate. 2. Bradykinin microinjections in different sites surrounding the Pa5 compromising the external cuneate nucleus, the trigeminal nucleus, the lateral and ventral spinal trigeminal tract and the dorsal trigeminal tract rostral and caudal to the Pa5 did not elicit significant pressor responses. In contrast, microinjections in the paratrigeminal nucleus produced pressor effects. Injections in the dorsolateral medulla directly over the paratrigeminal nucleus produced larger responses than when injections were made in the nucleus. Saline injections in the different nuclei did not produce pressor effects. 3. Neurochemical lesioning of the Pa5, with microinjections of ibotenic acid in the Pa5, abolished the pressor response to bradykinin injected over the lesioned nucleus. The effect was present, however, when bradykinin was injected on the contralateral side to the lesion, over the intact nucleus of the same animal. Pretreatment with capsaicin (injected in the lateral cerebral ventricle), which causes selective degeneration of afferent sensory fibres, did not alter the pressor effect of bradykinin injected over the paratrigeminal nucleus. 4. Dose-related responses were produced by different concentrations of bradykinin (0.6-1.8 pmol) microinjected over the nucleus. The bradykinin receptor antagonist HOE 140, injected over the paratrigeminal nucleus 30 min earlier, abolished the pressor response caused by bradykinin. 5. Low doses of bradykinin injected in or directly over the paratrigeminal nucleus increased arterial pressure and caused a small increase in heart rate by stimulating kinin receptors of the paratrigeminal nucleus in the dorsolateral medulla of awake and unrestrained rats. The pattern of the response was consistent with that of sympathetic stimulation. The paratrigeminal nucleus, which receives primary afferents and projects to the nucleus tractus solitarii and the rostral ventral lateral medulla, may be positioned as relay nucleus possibly connecting sensory input to structures that regulate blood pressure.
摘要
  1. 研究了大鼠延髓背外侧中三叉神经旁核(Pa5)在缓激肽引起的升压反应中的作用。向未麻醉大鼠的三叉神经旁核直接微量注射6皮摩尔缓激肽可使动脉压显著升高,心率适度增加。2. 在Pa5周围不同部位微量注射缓激肽,包括楔外核、三叉神经核、三叉神经脊髓束外侧和腹侧以及Pa5头端和尾端的三叉神经背束,均未引起显著的升压反应。相反,在三叉神经旁核内微量注射则产生升压效应。在延髓背外侧直接于三叉神经旁核上方注射比在核内注射产生的反应更大。在不同核团内注射生理盐水未产生升压效应。3. 向Pa5内微量注射鹅膏蕈氨酸对Pa5进行神经化学损伤,可消除在损伤核上方注射缓激肽引起的升压反应。然而,当在同一动物完整核的对侧注射缓激肽时,效应仍然存在。预先用辣椒素(注射到侧脑室)处理,导致传入感觉纤维选择性变性,并未改变在三叉神经旁核上方注射缓激肽的升压效应。4. 向核上方微量注射不同浓度(0.6 - 1.8皮摩尔)的缓激肽可产生剂量相关反应。提前30分钟在三叉神经旁核上方注射缓激肽受体拮抗剂HOE 140,可消除缓激肽引起的升压反应。5. 在清醒且不受束缚的大鼠延髓背外侧,向三叉神经旁核内或其上方注射低剂量缓激肽可通过刺激三叉神经旁核的激肽受体使动脉压升高,并使心率略有增加。反应模式与交感神经刺激一致。三叉神经旁核接受初级传入纤维并投射到孤束核和延髓头端腹外侧,可能作为一个中继核,将感觉输入与调节血压的结构相连接。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccb4/1159576/40e676d202c8/jphysiol00272-0123-a.jpg

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