Department of Cardiovascular and Renal Physiology and Pharmacology, School of Pharmaceutical Sciences, Universiti Sains Malaysia, Minden, Penang, Malaysia.
Ren Fail. 2010 Jan;32(1):96-102. doi: 10.3109/08860220903389196.
The role of renal sympathetic nerves in the pathogenesis of ischemic acute renal failure (ARF) and the immediate changes in the renal excretory functions following renal ischemia were investigated. Two groups of male Sprague Dawley (SD) rats were anesthetized (pentobarbitone sodium, 60 mg kg(-1) i.p.) and subjected to unilateral renal ischemia by clamping the left renal artery for 30 min followed by reperfusion. In group 1, the renal nerves were electrically stimulated and the responses in the renal blood flow (RBF) and renal vascular resistance (RVR) were recorded, while group 2 was used to study the early changes in the renal functions following renal ischemia. In post-ischemic animals, basal RBF and the renal vasoconstrictor reperfusion to renal nerve stimulation (RNS) were significantly lower (all p < 0.05 vs. control). Mean arterial pressure (MAP), basal RVR, urine flow rate (UFR), absolute and fractional excretions of sodium (U(Na)V and FE(Na)), and potassium (U(K)V and FE(K)) were higher in ARF rats (all p < 0.05 vs. control). Post-ischemic animals showed markedly lower glomerular filtration rate (GFR) (p < 0.05 vs. control). No appreciable differences were observed in urinary sodium to potassium ratio (U(Na)/U(K)) during the early reperfusion phase of renal ischemia (p > 0.05 vs. control). The data suggest an immediate involvement of renal sympathetic nerve action in the pathogenesis of ischemic ARF primarily through altered renal hemodynamics. Diuresis, natriuresis, and kaliuresis due to impaired renal tubular functions are typical responses to renal ischemia and of comparable magnitudes.
研究了肾交感神经在缺血性急性肾衰竭（ARF）发病机制中的作用以及肾缺血后肾脏排泄功能的即刻变化。将两组雄性 Sprague Dawley（SD）大鼠麻醉（戊巴比妥钠，60mgkg(-1) 腹腔注射），通过夹闭左肾动脉 30 分钟然后再灌注来进行单侧肾缺血。在第 1 组中，电刺激肾神经并记录肾血流量（RBF）和肾血管阻力（RVR）的反应，而第 2 组用于研究肾缺血后早期肾功能的变化。在缺血后的动物中，基础 RBF 和肾神经刺激（RNS）的肾血管收缩反应明显降低（均 p < 0.05 与对照组相比）。平均动脉压（MAP）、基础 RVR、尿流量率（UFR）、绝对和分数排泄钠（U（Na）V 和 FE（Na））以及钾（U（K）V 和 FE（K））在 ARF 大鼠中均升高（均 p < 0.05 与对照组相比）。缺血后动物的肾小球滤过率（GFR）明显降低（p < 0.05 与对照组相比）。在肾缺血的早期再灌注期间，尿钠与钾的比值（U（Na）/U（K））没有明显差异（p > 0.05 与对照组相比）。这些数据表明，肾交感神经活动的即刻参与主要通过改变肾脏血液动力学在缺血性 ARF 的发病机制中起作用。由于肾小管功能受损而导致的利尿、排钠和排钾是对肾缺血的典型反应，其程度相当。
