Wu Xiao Chun, Johns Edward J
Department of Physiology, The Medical School, Birmingham, United Kingdom.
Hypertension. 2002 Mar 1;39(3):790-3. doi: 10.1161/hy0302.105681.
This study investigated the role of NO in mediating the renal sympathetic nerve-mediated increases in proximal tubular fluid reabsorption (Jva). In inactin-anesthetized Wistar rats, renal sympathetic nerve stimulation (15 V, 2 ms) at 0.75 and 1.0 Hz did not change blood pressure or glomerular filtration rate but did decrease urine flow and sodium excretion in a frequency-related fashion by 40% to 50% at 1.0 Hz (both, P<0.01). Renal nerve stimulation in control animals increased Jva by 11% at 0.75 Hz (P<0.05) and 31% at 1.0 Hz (P<0.01). Intraluminal N(omega)-nitro-L-arginine methyl ester (L-NAME) resulted in a higher basal Jva (19%, P<0.05), and renal nerve stimulation had no effect on Jva. When L-NAME plus sodium nitroprusside was present intraluminally, however, there were frequency-dependent increases in Jva that were similar in pattern and magnitude to the control rats. Introduction of the relatively selective nNOS blocker 7-nitroindazole intraluminally, at 10(-6) and 10(-4) M, raised basal Jva by 18% and 24%, respectively (P<0.01), and renal nerve stimulation did not change Jva. Intraluminal aminoguanidine (10(-4) M), a relatively selective iNOS blocker, did not affect basal Jva, which remained unchanged during renal nerve stimulation. These data are consistent with NO exerting a tonic inhibitory action on the basal levels of Jva, which, in part, is caused by NO generated by the nNOS isoform. Moreover, the findings have revealed that the presence of NO is necessary to ensure that renal nerves can stimulate fluid reabsorption by the proximal tubules, requiring NO generated from both nNOS and iNOS.
本研究调查了一氧化氮（NO）在介导肾交感神经引起的近端肾小管液重吸收（Jva）增加中的作用。在经肌动蛋白麻醉的Wistar大鼠中，以0.75和1.0 Hz的频率进行肾交感神经刺激（15 V，2 ms）不会改变血压或肾小球滤过率，但会以频率相关的方式使尿流和钠排泄减少，在1.0 Hz时减少40%至50%（两者均P<0.01）。对照动物的肾神经刺激在0.75 Hz时使Jva增加11%（P<0.05），在1.0 Hz时增加31%（P<0.01）。管腔内注入N（ω）-硝基-L-精氨酸甲酯（L-NAME）导致基础Jva升高（19%，P<0.05），而肾神经刺激对Jva无影响。然而，当管腔内同时存在L-NAME和硝普钠时，Jva出现频率依赖性增加，其模式和幅度与对照大鼠相似。管腔内注入相对选择性的nNOS阻滞剂7-硝基吲唑，浓度为10（-6）和10（-4）M时，基础Jva分别升高18%和24%（P<0.01），肾神经刺激未改变Jva。管腔内注入相对选择性的iNOS阻滞剂氨基胍（10（-4）M）不影响基础Jva，在肾神经刺激期间基础Jva保持不变。这些数据与NO对Jva基础水平发挥紧张性抑制作用一致，部分原因是由nNOS亚型产生的NO所致。此外，研究结果表明，NO的存在对于确保肾神经能够刺激近端小管的液体重吸收是必要的，这需要nNOS和iNOS产生的NO。
