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孤束核中阻断心房利钠肽的升压效应。

Pressor effect of blocking atrial natriuretic peptide in nucleus tractus solitarii.

作者信息

Yang R H, Jin H K, Wyss J M, Chen Y F, Oparil S

机构信息

Department of Medicine, University of Alabama, Birmingham.

出版信息

Hypertension. 1992 Feb;19(2):198-205. doi: 10.1161/01.hyp.19.2.198.

Abstract

Previous studies have shown that microinjection of atrial natriuretic peptide into the caudal nucleus tractus solitarii produces significant increases in local neuronal firing rate associated with reductions in arterial pressure in anesthetized Wistar rats. Single units excited by microinjection of atrial natriuretic peptide into the caudal nucleus tractus solitarii were also excited by activation of arterial baroreceptors and inhibited by baroreceptor unloading. To test the hypothesis that endogenous atrial natriuretic peptide in caudal nucleus tractus solitarii is involved in the tonic control of blood pressure in the rat, we administered a blocking monoclonal antibody to atrial natriuretic peptide in a volume of 50 nl artificial cerebrospinal fluid via microinjection into the caudal nucleus tractus solitarii of spontaneously hypertensive and Wistar-Kyoto rats and observed the effects on mean arterial pressure and heart rate. Control injections of monoclonal antibody were administered into the rostral nucleus tractus solitarii, hypoglossal nucleus, spinal trigeminal nucleus, and cuneate nucleus of spontaneously hypertensive rats. Microinjection of monoclonal antibody into the caudal nucleus tractus solitarii caused significant increases in mean arterial pressure in spontaneously hypertensive rats but not in Wistar-Kyoto rats. There was no concomitant change in heart rate. Control injections of purified mouse immunoglobulin into the caudal nucleus tractus solitarii and of monoclonal antibody into the control neuronal groups listed above had no effect on mean arterial pressure. These results suggest that endogenous atrial natriuretic peptide in the caudal nucleus tractus solitarii mediates tonic control of blood pressure in spontaneously hypertensive rats but not in normotensive Wistar-Kyoto rats.

摘要

先前的研究表明,向麻醉的Wistar大鼠的孤束核尾侧亚核微量注射心房利钠肽会使局部神经元放电频率显著增加,同时动脉血压降低。向孤束核尾侧亚核微量注射心房利钠肽所兴奋的单个神经元,也会因动脉压力感受器的激活而兴奋,并因压力感受器负荷减轻而受到抑制。为了验证孤束核尾侧亚核中的内源性心房利钠肽参与大鼠血压的紧张性控制这一假说,我们通过微量注射,将50 nl人工脑脊液中的抗心房利钠肽阻断单克隆抗体注入自发性高血压大鼠和Wistar - Kyoto大鼠的孤束核尾侧亚核,并观察其对平均动脉压和心率的影响。将单克隆抗体对照注射到自发性高血压大鼠的孤束核头侧亚核、舌下神经核、三叉神经脊束核和楔束核。向自发性高血压大鼠的孤束核尾侧亚核微量注射单克隆抗体可使平均动脉压显著升高,但对Wistar - Kyoto大鼠则无此作用。心率没有随之改变。向孤束核尾侧亚核微量注射纯化的小鼠免疫球蛋白以及向上述对照神经元组微量注射单克隆抗体,对平均动脉压均无影响。这些结果表明,孤束核尾侧亚核中的内源性心房利钠肽介导自发性高血压大鼠的血压紧张性控制,但对正常血压的Wistar - Kyoto大鼠则无此作用。

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