Long-term captopril treatment. Angiotensin II receptors and responses.
Long-term captopril treatment. Angiotensin II receptors and responses.
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长期卡托普利治疗。
DOI：
10.1161/01.hyp.11.2_pt_2.i148
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Berecek,KH
中科院分区：
文献类型：
--
作者：
Wilson,KM;Magargal,W;Berecek,KH
本研究旨在探讨血管紧张素I（AngI）转换酶抑制剂卡托普利（Captopril）对自发性高血压大鼠（SHR）降压作用的机制。饮用反应，外周血管反应，血管紧张素II（Ang II）受体结合在大脑和血管平滑肌进行了检查，在控制和卡托普利治疗的SHR。妊娠期和哺乳期母鼠口服卡托普利（100 mg/kg）。断奶后，后代继续服用卡托普利（50 mg/kg）。与年龄匹配的对照组的169 +/- 4 mm Hg（男性）和162 +/- 2 mm Hg（女性）相比，卡托普利治疗21周后的平均收缩压为122 +/- 3 mm Hg（男性）和118 +/- 4 mm Hg（女性）。与对照SHR相比，Captopril治疗的SHR对脑室内（10 ng）和皮下（100微克/kg）给予Ang I和II的饮酒反应减弱。血管紧张素Ⅱ受体结合在下丘脑，丘脑，和间隔的卡托普利治疗SHR也显着减少。相反，抑郁的血管紧张素能系统在大脑中，外周血管反应性血管紧张素II，在隔离，人工灌注肾脏，测定升高。阈值和ED 50值血管紧张素II显着低于卡托普利治疗的SHR比对照组。血管紧张素II受体结合在主动脉平滑肌细胞制备的卡托普利治疗SHR也显着大于从控制的细胞。因此，终身治疗与巯甲丙脯酸诱导的外周和大脑中的肾素血管紧张素系统的变化，表现为受体结合和血管紧张素II的反应性的变化。（250字处删节）
The purpose of this study was to elucidate the mechanism of the antihypertensive effect of the angiotensin I (Ang I) converting enzyme inhibitor captopril in spontaneously hypertensive rats (SHR). Drinking responses, peripheral vascular reactivity, and angiotensin II (Ang II) receptor binding in both the brain and vascular smooth muscle were examined in control and captopril-treated SHR. Pregnant and nursing dams were treated with oral captopril (100 mg/kg). After weaning, offspring were maintained on captopril (50 mg/kg). The average systolic pressures after 21 weeks of captopril treatment were 122 +/- 3 mm Hg (male) and 118 +/- 4 mm Hg (female) as compared with 169 +/- 4 mm Hg (male) and 162 +/- 2 mm Hg (female) in age-matched controls. Drinking responses to intracerebroventricular (10 ng) and subcutaneous (100 micrograms/kg) administration of Ang I and II were attenuated in captopril-treated SHR in comparison to control SHR. Ang II receptor binding in the hypothalamus, thalamus, and septum of captopril-treated SHR was also significantly reduced. In contrast to a depressed angiotensinergic system in the brain, peripheral vascular reactivity to Ang II, as determined in isolated, artificially perfused kidneys, was elevated. Threshold and ED50 values for Ang II were significantly lower in captopril-treated SHR than in controls. Ang II receptor binding in aortic smooth muscle cells prepared from captopril-treated SHR was also significantly greater than in cells from controls. Thus, lifetime treatment with captopril induced alterations in the renin angiotensin systems in the periphery and brain that were manifested by changes in receptor binding and responsiveness to Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)