The antihypertensive effect of acute intracerebroventricular administration of captopril in Dahl salt-sensitive rats.
The antihypertensive effect of acute intracerebroventricular administration of captopril in Dahl salt-sensitive rats.
复制标题
卡托普利急性脑室内给药对达尔盐敏感大鼠的抗高血压作用。
DOI：
10.1016/0014-2999(92)90459-h
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发表时间：
1992
影响因子：
5
通讯作者：
Weyhenmeyer,JA
中科院分区：
文献类型：
--
作者：
Lark,LA;Weyhenmeyer,JA
在许多高血压动物模型中，已经证明了集中给药血管紧张素转换酶（ACE）抑制剂降低平均动脉压（MAP）的能力。在本研究中，我们评估了脑室内（i. c. v.）给清醒、自由活动的高血压近交系Dahl盐敏感（DS/JR）大鼠及其正常血压对照近交系Dahl盐耐受（DP/JR）大鼠注射血管紧张素转换酶抑制剂卡托普利（10 μg）。DS/JR和DR/JR大鼠从4周龄开始维持8%盐饮食直到7-8周龄的实验，此时DS/JR压力与DR/JR大鼠相比显著升高（分别为185 ± 6和99 ± 2 mm Hg）。给DS/JR大鼠静脉注射Captopril后，可观察到持续数小时的显著降压反应，最大降压幅度为17.6 ± 4.1 mm Hg。同样的处理对DR/JR大鼠的MAP没有影响。两组的平均动脉压均未受到单独的载体i. c. v.给药或通过静脉内（i. v.）给药100 μg卡托普利。这些发现表明，静脉注射Captopril可降低高血压DS/JR大鼠的MAP。进一步的研究将是必要的，以阐明这种降压作用的机制。
The ability of centrally administered angiotensin converting enzyme (ACE) inhibitors to lower mean arterial pressure (MAP) has been demonstrated in numerous animal models of hypertension. In the present study, we assessed the effect of intracerebroventricular (i.c.v.) injection of the ACE inhibitor captopril (10 μg) on MAP in conscious, freely moving hypertensive inbred Dahl salt-sensitive (DS/JR) rats and their normotensive control inbred Dahl salt-resistant (DP/JR) rats. Both DS/JR and DR/JR rats were maintained on an 8% salt diet from 4 weeks of age until experimentation at 7–8 weeks of age, at which time DS/JR pressures were significantly elevated as compared to DR/JR rats (185 ± 6 vs. 99 ± 2 mm Hg, respectively). Following i.c.v. administration of captopril, a significant depressor response lasting for several hours was observed in DS/JR rats, with a maximum reduction of 17.6 ± 4.1 mm Hg. The same treatment had no effect on the MAP of DR/JR rats. Mean arterial pressures in both groups were not significantly affected by i.c.v. administration of vehicle alone or by intravenous (i.v.) administration of 100 μg of captopril. These findings indicate that i.c.v. captopril lowers MAP in hypertensive DS/JR rats. Further studies will be necessary to elucidate the mechanism of this antihypertensive effect.