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血管紧张素II作为清醒大鼠脑干压力感受器反射的调节因子。

Angiotensin II as a modulator of baroreceptor reflexes in the brainstem of conscious rats.

作者信息

Michelini L C, Bonagamba L G

机构信息

Departamento de Fisiologia e Biofísica, Universidade de São Paulo, Brazil.

出版信息

Hypertension. 1990 Feb;15(2 Suppl):I45-50. doi: 10.1161/01.hyp.15.2_suppl.i45.

DOI:10.1161/01.hyp.15.2_suppl.i45
PMID:2298476
Abstract

The effect of microinjection into the nucleus tractus solitarii (NTS) of angiotensin II (Ang II) on baroreceptor control of heart rate (HR) in conscious, freely moving rats was evaluated with a new method of long-term cannulation of the dorsal brainstem areas. Reflex changes in HR were produced by intravenous bolus injections of either phenylephrine or sodium nitroprusside (0.2-25.6 micrograms/kg) both after saline and after unilateral microinjection of Ang II into the NTS (24 ng, 0.2 microliter) and compared with those produced after administration of Ang II into the fourth ventricle (24 ng, 0.2 microliter) or intravenously (1-2 ng/kg/min). Baseline levels of mean arterial pressure (MAP) and HR were not affected by the route of Ang II application but reflex bradycardia during MAP increase was significantly attenuated after injections of Ang II into the NTS. Both the slope and the intercept of the regression line function between delta HR and delta MAP were reduced by 43% from the control value of -1.55 +/- 0.13 beats/min/mm Hg (p less than 0.01) and -14 +/- 5 beats/min (p less than 0.05), respectively. Similar reductions were observed after Ang II administration into the fourth ventricle or intravenously, although microinjections into the cerebellum produced no effect. Endogenous blockade of Ang II by saralasin (22 ng) in the NTS facilitated the bradycardic response (-2.29 +/- 0.91 beats/min/mm Hg). Nitroprusside-induced tachycardia was not altered by Saralasin microinjection into the NTS or by Ang II application to the NTS, fourth ventricle, or intravenously.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

采用一种新的长期插管至背侧脑干区域的方法,评估了向清醒、自由活动大鼠孤束核(NTS)微量注射血管紧张素II(Ang II)对心率(HR)压力感受器控制的影响。在静脉推注去氧肾上腺素或硝普钠(0.2 - 25.6微克/千克)后,分别在注射生理盐水后以及向NTS单侧微量注射Ang II(24纳克,0.2微升)后,引发HR的反射性变化,并与向第四脑室注射Ang II(24纳克,0.2微升)或静脉注射(1 - 2纳克/千克/分钟)后产生的变化进行比较。平均动脉压(MAP)和HR的基线水平不受Ang II给药途径的影响,但在MAP升高期间,向NTS注射Ang II后,反射性心动过缓显著减弱。HR变化量(ΔHR)与MAP变化量(ΔMAP)之间回归线函数的斜率和截距分别比对照值-1.55±0.13次/分钟/毫米汞柱(p<0.01)和-14±5次/分钟(p<0.05)降低了43%。向第四脑室或静脉注射Ang II后也观察到类似的降低,尽管向小脑微量注射没有效果。NTS中沙拉新(22纳克)对Ang II的内源性阻断促进了心动过缓反应(-2.29±0.91次/分钟/毫米汞柱)。向NTS微量注射沙拉新或向NTS、第四脑室或静脉注射Ang II均未改变硝普钠诱导的心动过速。(摘要截断于250字)

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