Division of Renal and Vascular Physiology, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Biomedical Engineering, Department of Electrical Engineering, Technical University of Denmark, Lyngby, Denmark.
Acta Physiol (Oxf). 2015 Jul;214(3):402-14. doi: 10.1111/apha.12525. Epub 2015 May 29.
We tested the hypothesis that K(V)7 channels contribute to basal renal vascular tone and that they participate in agonist-induced renal vasoconstriction or vasodilation.
KV 7 channel subtypes in renal arterioles were characterized by immunofluorescence. Renal blood flow (RBF) was measured using an ultrasonic flow probe. The isometric tension of rat interlobar arteries was examined in a wire myograph. Mice afferent arteriolar diameter was assessed utilizing the perfused juxtamedullary nephron technique.
Immunofluorescence revealed that K(V)7.4 channels were expressed in rat afferent arterioles. The K(V)7 blocker XE991 dose-dependently increased the isometric tension of rat interlobar arteries and caused a small (approx. 4.5%) RBF reduction in vivo. Nifedipine abolished these effects. Likewise, XE991 reduced mouse afferent arteriolar diameter by approx. 5%. The K(V)7.2-5 stimulator flupirtine dose-dependently relaxed isolated rat interlobar arteries and increased (approx. 5%) RBF in vivo. The RBF responses to NE or Ang II administration were not affected by pre-treatment with XE991 or flupirtine. XE991 pre-treatment caused a minor augmentation of the acetylcholine-induced increase in RBF, while flupirtine pre-treatment did not affect this response.
It is concluded that K(V)7 channels, via nifedipine sensitive channels, have a role in the regulation of basal renal vascular tone. There is no indication that K(V)7 channels have an effect on agonist-induced renal vasoconstriction while there is a small effect on acetylcholine-induced vasodilation.
我们检验了假设，即 K(V)7 通道有助于基础肾血管张力，并参与激动剂诱导的肾血管收缩或舒张。
通过免疫荧光法对肾小动脉中的 KV7 通道亚型进行了特征描述。使用超声流量探针测量肾血流量 (RBF)。在wire myograph 中检查大鼠小叶间动脉的等长张力。利用灌流髓旁肾单位技术评估小鼠入球小动脉直径。
免疫荧光显示 K(V)7.4 通道在大鼠入球小动脉中表达。K(V)7 阻滞剂 XE991 呈剂量依赖性增加大鼠小叶间动脉的等长张力，并导致体内 RBF 减少约 4.5%。硝苯地平消除了这些作用。同样，XE991 使小鼠入球小动脉直径减少约 5%。K(V)7.2-5 激动剂 flupirtine 呈剂量依赖性地使分离的大鼠小叶间动脉松弛，并增加体内（约 5%）RBF。NE 或 Ang II 给药引起的 RBF 反应不受 XE991 或 flupirtine 预处理的影响。XE991 预处理导致 RBF 对乙酰胆碱诱导的增加有轻微增强，而 flupirtine 预处理不影响该反应。
K(V)7 通道通过硝苯地平敏感通道，在调节基础肾血管张力方面起作用。没有迹象表明 K(V)7 通道对激动剂诱导的肾血管收缩有影响，而对乙酰胆碱诱导的血管舒张有轻微影响。
