血管紧张素II对肾血管上皮钠通道蛋白的调节作用。
Angiotensin II regulation of renal vascular ENaC proteins.
作者信息
Jernigan Nikki L, Speed Joshua, LaMarca Babette, Granger Joey P, Drummond Heather A
机构信息
Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
出版信息
Am J Hypertens. 2009 Jun;22(6):593-7. doi: 10.1038/ajh.2009.59. Epub 2009 Mar 26.
BACKGROUND
The importance of beta and gamma epithelial Na(+) channel (ENaC) proteins in vascular smooth muscle cell (VSMC)-mediated pressure-induced constriction in renal interlobar arteries has been demonstrated recently. In renal epithelial tissue, ENaC expression is regulated by angiotensin II (Ang II). However, whether Ang II regulates vascular ENaC expression has never been determined. Therefore, the goal of the current investigation was to determine whether Ang II affects vascular ENaC expression and its contribution to pressure-induced constriction.
METHODS
To address this goal, Sprague-Dawley rats were infused with Ang II (50 ng/kg/min) via osmotic minipump for 1 week. Mean arterial pressure (MAP) was measured using radiotelemetry. Interlobar arteries were isolated from these animals to assess VSMC ENaC protein expression, pressure-induced constriction, and agonist induced vascular reactivity.
RESULTS
MAP was not different in control (113 +/- 2 mm Hg) and Ang II- (114 +/- 2 mm Hg) infused mice. We found that Ang II infusion decreased renal VSMC beta and gammaENaC immunolabeling by 18%. Consistent with this finding, we also found that ENaC-dependent peak pressure-induced constriction was inhibited from 38 +/- 3% to 25 +/- 1% at 125 mm Hg. Vasoreactivity to KCl, phenylephrine (PE), and acetylcholine (ACh) was unchanged.
CONCLUSIONS
Ang II suppression of pressure-induced constrictor responses in renal interlobar arteries may be mediated, at least in part, by inhibition of beta and gammaENaC protein expression.
背景
β和γ上皮钠通道（ENaC）蛋白在肾叶间动脉血管平滑肌细胞（VSMC）介导的压力诱导收缩中的重要性最近已得到证实。在肾上皮组织中，ENaC的表达受血管紧张素II（Ang II）调节。然而，Ang II是否调节血管ENaC的表达尚未确定。因此，本研究的目的是确定Ang II是否影响血管ENaC的表达及其对压力诱导收缩的作用。
方法
为实现这一目标，通过渗透微型泵给Sprague-Dawley大鼠输注Ang II（50 ng/kg/min），持续1周。使用无线电遥测法测量平均动脉压（MAP）。从这些动物中分离出叶间动脉，以评估VSMC ENaC蛋白表达、压力诱导的收缩以及激动剂诱导的血管反应性。
结果
对照组（113±2 mmHg）和输注Ang II组（114±2 mmHg）的小鼠MAP无差异。我们发现输注Ang II使肾VSMC的β和γ ENaC免疫标记减少了18%。与此发现一致，我们还发现，在125 mmHg时，ENaC依赖性峰值压力诱导的收缩从38±3%被抑制至25±1%。对氯化钾、去氧肾上腺素（PE）和乙酰胆碱（ACh）的血管反应性未改变。
结论
Ang II对肾叶间动脉压力诱导的收缩反应的抑制作用可能至少部分是由β和γ ENaC蛋白表达的抑制介导的。
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