Blood pressure response to chronic episodic hypoxia: the renin-angiotensin system
Blood pressure response to chronic episodic hypoxia: the renin-angiotensin system
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DOI：
10.1152/japplphysiol.00152.2001
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发表时间：
2002-02-01
影响因子：
3.3
通讯作者：
Bader, M
中科院分区：
文献类型：
--
作者：
Fletcher, EC;Orolinova, N;Bader, M
通过使用吸入的氧分数，产生相当于在人类睡眠呼吸暂停中看到的氧合血红蛋白去饱和，我们已经证明，35天的反复发作性缺氧（每30秒，7小时/天）的结果在8-13毫米汞柱持续增加昼夜系统平均动脉血压（MAP）在大鼠。血管紧张素II受体（AT（1a））的阻断消除了这种反应。各组雄性Sprague-Dawley大鼠喂食高盐（8%）、随意盐或低盐（0.1%）饮食7周：2周洗入用于基线血压测量，5周实验条件。在每个盐组的大鼠进行间歇性缺氧，而对照组在常氧条件下保持未处理。MAP保持在所有nonepisodic缺氧控制以及高盐饮食的episodic缺氧暴露大鼠的基础水平。自由和低盐间歇性缺氧大鼠的MAP分别从基线时的106和104 mmHg增加到112和113 mmHg（P < 0.05）。在高盐对照组和间歇性缺氧组大鼠，全肾肾素mRNA被抑制，而肾AT 1a mRNA则表现出相反的变化。高盐饮食对肾素-血管紧张素系统的抑制阻断了间歇性缺氧大鼠MAP的增加，部分是通过抑制局部组织的肾素水平。组织血管紧张素II系统的上调似乎是必要的慢性血压变化，发生从间歇性缺氧。
By using an inspired oxygen fraction that produces oxyhemoglobin desaturation equivalent to that seen in human sleep apnea, we have demonstrated that 35 days of recurrent episodic hypoxia (every 30 s for 7 h/day) results in an 8-13 mmHg persistent increase in diurnal systemic mean arterial blood pressure (MAP) in rats. Blockade of angiotensin II receptors (AT(1a)) eliminates this response. Separate groups of male Sprague-Dawley rats were fed high-salt (8%), ad libitum-salt, or low-salt (0.1%) diets for 7 wk: 2 wk of wash-in for baseline blood pressure measurement and 5 wk of experimental conditions. Rats in each salt group were subjected to episodic hypoxia whereas controls remained unhandled under normoxic conditions. MAP remained at basal levels in all nonepisodic hypoxia controls as well as high-salt-diet episodic hypoxia-exposed rats. Ad lib and low-salt episodic hypoxia rats showed an increase in MAP from 106 and 104 mmHg at baseline to 112 and 113 mmHg, respectively (P < 0.05). Whole kidney renin mRNA was suppressed in high-salt controls and episodic hypoxia rats, whereas kidney AT1a mRNA showed opposite changes. Suppression of the renin-angiotensin system with a high-salt diet blocks the increase in MAP in episodic hypoxia-challenged rats, in part by suppressing local tissue renin levels. Upregulation of the tissue angiotensin II system appears to be necessary for the chronic blood pressure changes that occur from episodic hypoxia.