Division of Renal and Vascular Physiology, Department of Biomedical Sciences, The Panum Institute, University of Copenhagen, Denmark.
Acta Physiol (Oxf). 2011 Aug;202(4):703-12. doi: 10.1111/j.1748-1716.2011.02304.x. Epub 2011 May 27.
We investigated the mechanisms behind K(+) -induced renal vasodilation in vivo in normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR).
Renal blood flow (RBF) was measured utilizing an ultrasonic Doppler flow probe. Renal vascular resistance (RVR) was calculated as the ratio of mean arterial pressure (MAP) and RBF (RVR = MAP/RBF). Test drugs were introduced directly into the renal artery. Inward rectifier K(+) (K(ir) ) channels and Na(+) ,K(+) -ATPase were blocked by Ba(2+) and ouabain (estimated plasma concentrations ∼20 and ∼7 μm) respectively.
Confocal immunofluorescence microscopy demonstrated K(ir) 2.1 channels in pre-glomerular vessels of SD and SHR. Ba(2+) caused a transient (6-13%) increase in baseline RVR in both SD and SHR. Ouabain had a similar effect. Elevated renal plasma [K(+) ] (∼12 mm) caused a small and sustained decrease (5-13%) in RVR in both strains. This decrease was significantly larger in SHR than in SD. The K(+) -induced vasodilation was attenuated by Ba(2+) in control SD and SHR and by ouabain in SD. Nitric oxide (NO) blockade using l-NAME treatment increased MAP and decreased RBF in both rat strains, but did not affect the K(+) -induced renal vasodilation.
K(+) -induced renal vasodilation is larger in SHR, mediated by K(ir) channels in SD and SHR, and in addition, by Na(+) ,K(+) -ATPase in SD. In addition, NO is not essential for K(+) -induced renal vasodilation.
我们研究了在正常血压的 Sprague-Dawley（SD）大鼠和自发性高血压大鼠（SHR）体内 K(+) 诱导的肾血管舒张的机制。
利用超声多普勒血流探头测量肾血流量（RBF）。肾血管阻力（RVR）计算为平均动脉压（MAP）与 RBF 的比值（RVR = MAP/RBF）。测试药物直接引入肾动脉。内向整流钾（K(ir)）通道和 Na(+),K(+) -ATP 酶分别被 Ba(2+) 和哇巴因阻断（估计血浆浓度分别为 ∼20 和 ∼7 μm）。
共聚焦免疫荧光显微镜显示 SD 和 SHR 的肾小球前血管存在 K(ir) 2.1 通道。Ba(2+) 引起 SD 和 SHR 基础 RVR 短暂（6-13%）增加。哇巴因也有类似的作用。升高的肾血浆 [K(+) ]（∼12 mm）导致两种品系的 RVR 持续下降（5-13%）。SHR 的下降幅度明显大于 SD。在对照 SD 和 SHR 中，Ba(2+) 减弱了 K(+) 诱导的血管舒张，在 SD 中，哇巴因减弱了 K(+) 诱导的血管舒张。使用 l-NAME 处理阻断一氧化氮（NO）后，两种大鼠的 MAP 升高，RBF 降低，但不影响 K(+) 诱导的肾血管舒张。
SHR 的 K(+) 诱导的肾血管舒张更大，在 SD 和 SHR 中由 K(ir) 通道介导，在 SD 中还由 Na(+),K(+) -ATP 酶介导。此外，NO 对 K(+) 诱导的肾血管舒张不是必需的。
