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心房利钠肽调节自发性高血压大鼠的压力感受器反射。

Atrial natriuretic peptide modulates baroreceptor reflex in spontaneously hypertensive rat.

作者信息

Jin H, Yang R H, Calhoun D A, Wyss J M, Oparil S

机构信息

Department of Medicine, University of Alabama, Birmingham.

出版信息

Hypertension. 1992 Sep;20(3):374-9. doi: 10.1161/01.hyp.20.3.374.

Abstract

Our previous studies have suggested that atrial natriuretic peptide in the caudal nucleus tractus solitarii is involved in the centrally mediated regulation of blood pressure in the salt-sensitive spontaneously hypertensive rat (SHR). The current study tested the hypothesis that endogenous atrial natriuretic peptide in the caudal nucleus tractus solitarii participates in baroreceptor reflex control of heart rate in this hypertensive model. Salt-sensitive SHR and control Wistar-Kyoto (WKY) rats maintained on basal (1%) salt intake were studied. Arterial baroreceptor reflex-mediated changes in heart rate were recorded in conscious unrestrained rats during phenylephrine (5-40 micrograms.kg-1.min-1 infusion; 30 minutes later, atrial natriuretic peptide (50 ng), monoclonal antibody to atrial natriuretic peptide (0.55 micrograms), purified mouse immunoglobulin G (0.55 micrograms), or artificial cerebrospinal fluid vehicle (50 nl) was microinjected into the caudal nucleus tractus solitarii. Phenylephrine infusion was then repeated and mean arterial pressure and heart rate were monitored as before. The slope of the heart rate/mean arterial pressure relation was significantly less (p less than 0.05) in the salt-sensitive SHR than in the WKY control, indicating that baroreceptor reflex control of heart rate was blunted in this hypertensive model. Microinjection of atrial natriuretic peptide into the caudal nucleus tractus solitarii further blunted (p less than 0.05) baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats. In contrast, microinjection of the monoclonal antibody enhanced the sensitivity of baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们之前的研究表明,孤束核尾侧亚核中的心房利钠肽参与盐敏感型自发性高血压大鼠(SHR)的中枢介导的血压调节。本研究检验了以下假设:孤束核尾侧亚核中的内源性心房利钠肽参与该高血压模型中压力感受器对心率的反射控制。研究了维持基础(1%)盐摄入量的盐敏感型SHR和对照Wistar-Kyoto(WKY)大鼠。在清醒自由活动的大鼠中,记录去氧肾上腺素(5 - 40微克·千克⁻¹·分钟⁻¹输注;30分钟后,将心房利钠肽(50纳克)、心房利钠肽单克隆抗体(0.55微克)、纯化的小鼠免疫球蛋白G(0.55微克)或人工脑脊液载体(50纳升)微量注射到孤束核尾侧亚核中。然后重复去氧肾上腺素输注,并如前监测平均动脉压和心率。盐敏感型SHR中,心率/平均动脉压关系的斜率显著低于WKY对照(p < 0.05),表明该高血压模型中压力感受器对心率的反射控制减弱。向孤束核尾侧亚核微量注射心房利钠肽,进一步减弱了盐敏感型SHR中压力感受器对心率的反射控制(p < 0.05),但对WKY大鼠无此作用。相反,微量注射单克隆抗体增强了盐敏感型SHR中压力感受器对心率的反射控制敏感性,但对WKY大鼠无此作用。(摘要截短于250词)

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