Brain angiotensin II and baroreceptor reflex function in spontaneously hypertensive rats.
Brain angiotensin II and baroreceptor reflex function in spontaneously hypertensive rats.
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自发性高血压大鼠的脑血管紧张素 II 和压力感受器反射功能。
DOI：
10.1161/01.hyp.14.3.274
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Berecek,KH
中科院分区：
文献类型：
--
作者：
Cheng,SW;Kirk,KA;Robertson,JD;Berecek,KH
我们研究了之前报道的终生卡托普利治疗的自发性高血压大鼠(SHR)压力感受器反射功能的增加是否是由于脑血管紧张素II机制的抑制。孕期和哺乳期SHR口服卡托普利(100 mg/kg/d)。断奶后，仔鼠继续服用卡托普利(50 mg/kg/d)，直到研究(19-21周)。对照组大鼠饮用自来水。研究前一周，卡托普利治疗组和对照组SHR分别脑室注射血管紧张素II(7.5 ng/小时，渗透泵)或赋形剂(人工脑脊液)。压力感受器反射对心率的控制是通过平均动脉压(Mm Hg)变化与脉搏间期(毫秒搏动-1)变化之间的关系的斜率来评估的。动脉压分别通过静脉推注苯肾上腺素或硝普钠升高或降低。中心静脉注射血管紧张素II对自发性高血压患者和对照组的平均动脉压无显著影响(卡托普利-血管紧张素II 125+/-4vs.卡托普利-载药组121+/-2；对照组-血管紧张素II169+/-5vs.173+/-7 mm Hg)，但可显著增加基础心率(卡托普利-血管紧张素Ⅱ371+/-10vs卡托普利-载药组323+/-8，p<0.0002；对照-血管紧张素II338+/-7与对照载体312+/-8次/分钟，p<0.0183)和每日摄水量(卡托普利-血管紧张素II 20.7+/-2.2vs卡托普利9.8+/-0.7，p<0.0426；对照-血管紧张素II 33.1+/-3.8vs对照-载体9.0+/-0.6ml/100g体重，p<0.0001)。
We examined whether the increase in baroreceptor reflex function previously reported in lifetime - captopril-treated spontaneously hypertensive rats (SHR) was due to an inhibition of brain angiotensin II mechanisms. Pregnant and lactating SHR were given oral captopril (100 mg/kg/day). After weaning, pups were maintained on captopril (50 mg/kg/day) until the study (19-21 weeks). Control rats received tap water. One week before study captopril-treated and control SHR were given an intracerebroventricular infusion of angiotensin II (7.5 ng/hr, osmotic pump) or vehicle (artificial cerebrospinal fluid). Baroreceptor reflex control of heart rate was assessed by the slope of the relation between the change in mean arterial pressure (mm Hg) versus the change in pulse interval (msec beat-1). Arterial pressure was raised or lowered by intravenous bolus injections of phenylephrine or nitroprusside, respectively. Central infusion of angiotensin II had no significant effect on mean arterial pressure in captopril or control SHR (captopril-angiotensin II 125 +/- 4 vs. captopril-vehicle 121 +/- 2; control-angiotensin II 169 +/- 5 vs. control-vehicle 173 +/- 7 mm Hg), but it produced a significant rise in basal heart rate (captopril-angiotensin II 371 +/- 10 vs. captopril-vehicle 323 +/- 8, p less than 0.0002; control-angiotensin II 338 +/- 7 vs. control-vehicle 312 +/- 8 beats/min, p less than 0.0183) and in daily water intake (captopril-angiotensin II 20.7 +/- 2.2 vs. captopril-vehicle 9.8 +/- 0.7, p less than 0.0426; control-angiotensin II 33.1 +/- 3.8 vs. control-vehicle 9.0 +/- 0.6 ml/100 g body wt, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)