Attenuated afferent arteriolar response to acetylcholine in Goldblatt hypertension.
Attenuated afferent arteriolar response to acetylcholine in Goldblatt hypertension.
复制标题
戈德布拉特高血压患者传入小动脉对乙酰胆碱的反应减弱。
DOI：
10.1161/01.hyp.19.6.785
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Carmines,PK
中科院分区：
文献类型：
--
作者：
Ortenberg,JM;Cook,AK;Inscho,EW;Carmines,PK
我们测试的假设，即内皮依赖性传入小动脉血管舒张受损的非夹肾两肾，一个剪辑Goldblatt高血压大鼠相对于假手术对照。在左肾动脉上放置0.25 mm夹子后5 - 6周，Goldblatt大鼠的平均收缩压为173 +/- 10 mm Hg，对照组为118 +/- 4 mm Hg（p <0.01）。取右肾，采用离体血灌注肾髓质肾单位技术进行微血管影像测量研究。Goldblatt和对照大鼠的肾脏分别在150和110 mm Hg的肾动脉压下灌注。对照组（20.3 +/- 0.7微米）和Goldblatt组（21.1 +/- 1.7微米）肾脏的输入小动脉内径无差异。测定对增加浓度的内皮依赖性血管扩张剂乙酰胆碱（1 nM至10 μ M）的传入反应，揭示了Goldblatt大鼠剂量-反应关系的右移。当暴露于1 nM乙酰胆碱时，对照肾脏的传入小动脉显著扩张，而Goldblatt大鼠的小动脉扩张需要1,000倍的浓度。硝普钠是一种非内皮依赖性血管扩张剂，在两组中增加传入直径的程度相似。在另一组正常肾脏中，10 μ M乙酰胆碱的血管舒张反应被1,000 μ M硝基-L-精氨酸完全阻断，硝基-L-精氨酸是一种一氧化氮合成抑制剂。因此，内皮依赖性传入血管舒张似乎受损的Goldblatt高血压大鼠的非夹肾。这种现象可能导致Goldblatt高血压的肾脏血流动力学状态改变。
We tested the hypothesis that endothelium-dependent afferent arteriolar vasodilation is impaired in the nonclipped kidney of two-kidney, one clip Goldblatt hypertensive rats relative to sham-operated controls. Five to six weeks after positioning of a 0.25-mm clip on the left renal artery, systolic pressure averaged 173 +/- 10 mm Hg in Goldblatt rats and 118 +/- 4 mm Hg in controls (p less than 0.01). The right kidney was harvested for videometric study of the microvasculature using the in vitro blood-perfused juxtamedullary nephron technique. Kidneys from Goldblatt and control rats were perfused at renal arterial pressures of 150 and 110 mm Hg, respectively. Afferent arteriolar inside diameter did not differ between control (20.3 +/- 0.7 microns) and Goldblatt (21.1 +/- 1.7 microns) kidneys. Determination of afferent responses to increasing concentrations of the endothelium-dependent vasodilator acetylcholine (1 nM to 10 microM) in the bathing solution unveiled a shift to the right in the dose-response relation in Goldblatt rats. Afferent arterioles from control kidneys dilated significantly when exposed to 1 nM acetylcholine, whereas a 1,000-fold higher concentration was required to dilate arterioles from Goldblatt rats. Sodium nitroprusside, an endothelium-independent vasodilator, increased afferent diameter to a similar extent in both groups. In a separate group of normal kidneys, vasodilator responses to 10 microM acetylcholine were completely blocked by 1,000 microM nitro-L-arginine, an inhibitor of nitric oxide synthesis. Thus, endothelium-dependent afferent vasodilation appears to be impaired in the nonclipped kidney of Goldblatt hypertensive rats. This phenomenon could contribute to the altered renal hemodynamic status characteristic of Goldblatt hypertension.