Role of renal nerves in afferent arteriolar reactivity in angiotensin-induced hypertension.
Role of renal nerves in afferent arteriolar reactivity in angiotensin-induced hypertension.
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肾神经在血管紧张素诱导的高血压传入小动脉反应性中的作用。
DOI：
10.1161/01.hyp.29.1.442
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Navar,LG
中科院分区：
文献类型：
--
作者：
Ichihara,A;Inscho,EW;Imig,JD;Michel,RE;Navar,LG
本研究的目的是确定肾神经对血管紧张素 II (Ang II) 诱导的高血压中观察到的传入小动脉反应性增强的贡献。将未切除肾的 Sprague-Dawley 大鼠分为四组：假手术大鼠、去肾神经大鼠、输注 Ang II（40 ng/min，持续 13 天）大鼠和输注 Ang II+去肾神经大鼠。通过使用植入的动脉导管，监测清醒大鼠的平均动脉压（MAP）。 Ang II 输注导致 MAP 从 98±1（第 0 天）逐渐增加至 166±7 mm Hg（第 13 天）。 MAP 的增加在去神经大鼠中减弱，第 13 天平均为 136±3 mm Hg。第 13 天收获肾脏用于微循环实验或测量肾内 Ang II 水平。所有组的基底传入动脉直径相似，组平均值为 19.6 至 20.7 μm。慢性 Ang II 输注会增加肾内 Ang II 水平。去肾神经并没有改变这种效果。将灌注压从 100 毫米汞柱增加到 160 毫米汞柱，使假手术组的传入小动脉直径显着减少 11.2±0.6%，其余三组的程度相似。假手术组灌注Ang II (10 nmol/L)使传入小动脉直径减少34.3±2.0%。这种反应在注入 Ang II 的大鼠中增强 (62.3±3.4%)，但在去肾神经或 Ang II 注入 + 去肾神经的大鼠中没有增强。此外，传入小动脉对血管紧张素II的反应性增强不受肾上腺素能受体阻断的影响。与假手术对照组相比，去肾神经、输注 Ang II 和输注 Ang II+去肾神经的大鼠的传入小动脉对去甲肾上腺素的反应增强。钙离子载体 A23187 的给药在所有四组中均类似地减少了传入小动脉直径。这些结果表明，肾神经有助于高血压的发生以及慢性Ang II输注引起的传入小动脉对Ang II的反应性增强。
The objective of this study was to determine the contribution of renal nerves to the enhanced afferent arteriolar reactivity observed in angiotensin II (Ang II)-induced hypertension. Uninephrectomized Sprague-Dawley rats were divided into four groups: sham rats, renal-denervated rats, Ang II-infused (at 40 ng/min for 13 days) rats, and Ang II-infused+renal-denervated rats. With the use of an implanted arterial catheter, mean arterial pressure (MAP) was monitored in conscious rats. Ang II infusion resulted in a progressive increase in MAP from 98±1 (day 0) to 166±7 mm Hg (day 13). This increase in MAP was attenuated in denervated rats and averaged 136±3 mm Hg on day 13. Kidneys were harvested on day 13 for microcirculatory experiments or measurement of intrarenal Ang II levels. Basal afferent arteriolar diameter was similar in all groups, and group averages ranged from 19.6 to 20.7 μm. Chronic Ang II infusion increased intrarenal Ang II levels. Renal denervation did not alter this effect. Increasing perfusion pressure from 100 to 160 mm Hg reduced afferent arteriolar diameter significantly by 11.2±0.6% in the sham group and by a similar degree in the remaining three groups. Superfusion with Ang II (10 nmol/L) reduced afferent arteriolar diameter by 34.3±2.0% in the sham group. This response was enhanced in Ang II-infused (62.3±3.4%) but not in renal-denervated or Ang II-infused+renal-denervated rats. Additionally, the enhanced afferent arteriolar reactivity to Ang II was not influenced by adrenergic receptor blockade. The afferent arteriolar response to norepinephrine was enhanced in renal-denervated, Ang II-infused, and Ang II-infused+renal-denervated rats compared with sham controls. Administration of the calcium ionophore A23187 decreased afferent arteriolar diameter similarly in all four groups. These results indicate that renal nerves contribute to the development of hypertension and to the enhanced afferent arteriolar responsiveness to Ang II elicited by chronic Ang II infusion.