Sustained influence of the renal nerves to attenuate sodium retention in angiotensin hypertension
Sustained influence of the renal nerves to attenuate sodium retention in angiotensin hypertension
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DOI：
10.1152/ajpregu.2001.281.2.r434
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发表时间：
2001-08-01
影响因子：
2.8
通讯作者：
Hildebrandt, DA
中科院分区：
文献类型：
--
作者：
Lohmeier, TE;Lohmeier, JR;Hildebrandt, DA
最近的研究表明，肾交感神经活动的压力反射抑制持续长达5天的ANG II输注;然而，稳态条件与这种短时间的ANG II高血压无关。因此，本研究的主要目的是确定慢性静脉输注ANG II期间神经诱导的肾排泄功能增加是否在高血压稳定且达到钠平衡的更慢性条件下持续。实验进行了五个清醒的狗进行单侧肾去神经和手术分割膀胱成半膀胱，允许单独的24小时尿液收集去神经支配（登）和神经支配（Inn）的肾脏。ANG II在对照测量后以5 ng的速率输注10天。kg（-1）。min（-1）。24小时平均动脉压（MAP）和Den和Inn肾脏尿钠排泄率（Den/Inn）的对照值分别为92 +/- 4 mmHg和0.99 +/- 0.05。在ANG II输注的第8-10天，MAP稳定（+30 +/- 3 mmHg），并达到钠平衡。尽管在对照期间从肾脏排泄等量的钠，但在整个ANG II输注期间，从Inn肾脏排泄的钠速率大于Den肾脏（第10天Den/Inn钠= 0.56 +/- 0.05），表明肾交感神经活性的慢性抑制。在肾交感神经抑制期间，Inn与Den肾脏中的钠排泄速率更大，这也揭示了Den肾脏中钠排泄的潜在损害。虽然钠和一氧化氮（NO）的主要代谢产物的Den/Inn在ANG II高血压期间平行下降，但cGMP（NO的第二信使）的Den/Inn在整个研究期间保持在对照水平。这种差异不能支持这样的观点，即肾内NO产生和作用的缺乏导致钠排泄受损。最重要的是，这些结果支持的论点，肾交感神经活动的压力反射抑制持续在慢性血管紧张素II高血压，反应，可能发挥重要作用，在衰减动脉压的上升。
Recent studies indicate that baroreflex suppression of renal sympathetic nerve activity is sustained for up to 5 days of ANG II infusion; however, steady-state conditions are not associated with ANG II hypertension of this short duration. Thus the major goal of this study was to determine whether neurally induced increments in renal excretory function during chronic intravenous infusion of ANG II are sustained under more chronic conditions when hypertension is stable and sodium balance is achieved. Experiments were conducted in five conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. ANG II was infused after control measurements for 10 days at a rate of 5 ng . kg(-1) . min(-1). Twenty-four-hour control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from Den and Inn kidneys (Den/Inn) were 92 +/- 4 mmHg and 0.99 +/- 0.05, respectively. On days 8-10 of ANG II infusion, MAP was stable (+30 +/- 3 mmHg) and sodium balance was achieved. Whereas equal amounts of sodium were excreted from the kidneys during the control period, throughout ANG II infusion there was a greater rate of sodium excretion from Inn vs. Den kidneys (day 10 Den/Inn sodium = 0.56 +/- 0.05), indicating chronic suppression of renal sympathetic nerve activity. The greater rate of sodium excretion in Inn vs. Den kidneys during renal sympathoinhibition also revealed a latent impairment in sodium excretion from Den kidneys. Although the Den/Inn for sodium and the major metabolites of nitric oxide (NO) decreased in parallel during ANG II hypertension, the Den/Inn for cGMP, a second messenger of NO, remained at control levels throughout this study. This disparity fails to support the notion that a deficiency in NO production and action in Den kidneys accounts for the impaired sodium excretion. Most importantly, these results support the contention that baroreflex suppression of renal sympathetic nerve activity is sustained during chronic ANG II hypertension, a response that may play an important role in attenuating the rise in arterial pressure.