卡托普利避免高血压,血浆血管紧张素II升高,但增加血管紧张素1-7和血管紧张素II诱导的SHR离体肾灌注压

P. Castro-Moreno, J. P. Pardo, R. Hernández-Muñoz, J. J. López-Guerrero, L. Del Valle-Mondragón, G. Pastelín-Hernández, M. Ibarra-Barajas, R. Villalobos-Molina
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引用次数: 26

摘要

我们研究了ACE抑制剂卡托普利对高血压发展、Ang II和Ang-(1-7)血浆浓度、Ang II诱导的离体肾脏收缩以及自发性高血压(SHR)大鼠肾脏AT1R的影响。5周龄SHR和Wistar Kyoto (WKY)大鼠按30 mg/kg/天剂量给予卡托普利,连续饮水2周或14周。测量收缩压(SBP),检测离体肾脏的灌注压和AT1R表达;测定血浆中Ang II和Ang-(1-7)的浓度。卡托普利不改变WKY大鼠的收缩压,并避免其随着SHR年龄的增长而升高。SHR大鼠血浆Ang-II浓度升高~ 4-5倍,卡托普利可使其降低(P <0.05);而卡托普利在所有大鼠组中使Ang-(1-7)增加约2倍。卡托普利增加了WKY和SHR大鼠肾脏中Ang ii诱导的升压反应,而在α1-肾上腺素受体激动剂苯肾上腺素刺激的肾脏中没有观察到这种现象。卡托普利对不同品系和年龄的大鼠肾皮质和髓质的AT1R没有改变。数据显示,卡托普利通过阻断血管紧张素II的合成,增加了WKY和SHR大鼠的肾灌注压,但没有增加AT1R密度;然而,ACE抑制剂可能有其他作用,如激活信号传导过程,这可能有助于它们的不同效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Captopril avoids hypertension, the increase in plasma angiotensin II but increases angiotensin 1–7 and angiotensin II-induced perfusion pressure in isolated kidney in SHR

  1. We investigated captopril effects, an ACE inhibitor, on hypertension development, on Ang II and Ang-(1-7) plasma concentrations, on Ang II-induced contraction in isolated kidneys, and on kidney AT1R from spontaneously hypertensive (SHR) rats.
  2. Five weeks-old SHR and Wistar Kyoto (WKY) rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 or 14 weeks. Systolic blood pressure (SBP) was measured, and isolated kidneys were tested for perfusion pressure and AT1R expression; while Ang II and Ang-(1-7) concentrations were determined in plasma.
  3. Captopril did not modify SBP in WKY rats and avoided its increase as SHR aged. Plasma Ang-II concentration was ∼4-5 folds higher in SHR rats, and captopril reduced it (P < 0.05); while captopril increased Ang-(1-7) by ∼2 fold in all rat groups.
  4. Captopril increased Ang II-induced pressor response in kidneys of WKY and SHR rats, phenomenon not observed in kidneys stimulated with phenylephrine, a α1-adrenoceptor agonist.
  5. Captopril did not modify AT1R in kidney cortex and medulla among rat strains and ages.
  6. Data indicate that captopril increased Ang II-induced kidney perfusion pressure but not AT1R density in kidney of WKY and SHR rats, due to blockade of angiotensin II synthesis; however, ACE inhibitors may have other actions like activating signaling processes that could contribute to their diverse effects.
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