Chronic angiotensin II infusion causes differential responses in regional sympathetic nerve activity in rats.
Chronic angiotensin II infusion causes differential responses in regional sympathetic nerve activity in rats.
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DOI：
10.1161/hypertensionaha.109.145110
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发表时间：
2010-03
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影响因子：
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通讯作者：
Osborn JW
中科院分区：
文献类型：
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作者：
Yoshimoto M;Miki K;Fink GD;King A;Osborn JW
血管紧张素II(AngII)诱导的实验动物高血压被认为部分是由于交感神经系统的激活。这种交感神经激活似乎在食用高盐饮食的动物(血管盐性高血压)中得到加强。然而，交感神经活动的准确量化是困难的，争议仍然存在。一个特别重要的问题是：在血管盐性高血压患者中，交感神经活性(SNA)增加所针对的关键血管床是什么？为了解决这一问题，在5天的控制期、11天的血管紧张素转换酶抑制剂(150 ng/kg/min，sc)和5天的恢复期内，连续记录清醒大鼠的平均动脉压(MAP)和肾脏(RSNA)或腰椎SNA(LSNA)。在Angii期结束时，MAP达到了比对照水平高30-35 mm Hg的新的稳态水平，而RSNA在Angii的前7天下降了40%，然后在Angii的第10天恢复到对照水平。相比之下，LSNA在整个安吉时期都保持在控制水平。在另一项实验中，我们测量了正常(0.4%)或高盐(2.0%)饮食的清醒大鼠在服用血管紧张素转换酶之前和期间的后肢去甲肾上腺素(NE)溢出。两组血管紧张素Ⅱ对后肢NE外溢均无显著影响。我们得出结论，慢性血管紧张素Ⅱ对高盐饮食大鼠的肾脏和腰椎SNA有不同的调节作用，大鼠的血管紧张素Ⅱ高血压不是由肾脏或后肢血管床的SNA增加引起的。
Angiotensin II (AngII) – induced hypertension in experimental animals has been proposed to be due in part to activation of the sympathetic nervous system. This sympathetic activation appears to be accentuated in animals consuming a high salt diet (AngII-salt hypertension). However, accurate quantification of sympathetic activity is difficult and controversy remains. A particularly important question is: What are the critical vascular beds targeted by increased sympathetic nerve activity (SNA) in AngII-salt hypertension? To address this issue, mean arterial pressure (MAP) and renal (RSNA) or lumbar SNA (LSNA) were continuously recorded during a 5 day control period, 11 days of AngII (150 ng/kg/min, sc) and a 5 day recovery period in conscious rats on a high salt (2% NaCl) diet. Whereas MAP reached a new steady-state level of 30-35 mmHg above control levels by the end of the AngII period, RSNA decreased by 40% during the first 7 days of AngII and then returned towards control levels by day 10 of AngII. In contrast, LSNA remained at control levels throughout the AngII period. In another experiment we measured hindlimb norepinephrine (NE) spillover in conscious rats on normal (0.4%) or high (2.0%) salt diets before and during 14 days of AngII administration. AngII had no significant affect on hindlimb NE spillover in either group. We conclude that chronic AngII modulates renal and lumbar SNA differentially in rats consuming a high salt diet and that AngII-salt hypertension in the rat is not caused by increased SNA to the renal or hindlimb vascular beds.