Veiga Glaucia L, Nishi Erika E, Estrela Heder F, Lincevicius Gisele S, Gomes Guiomar N, Simões Sato Alex Y, Campos Ruy R, Bergamaschi Cássia T
Cardiovascular Division, Department of Physiology, Universidade Federal de São Paulo, Brazil.
Renal Division, Department of Physiology, Universidade Federal de São Paulo, Brazil.
Auton Neurosci. 2017 May;204:81-87. doi: 10.1016/j.autneu.2016.11.006. Epub 2016 Dec 1.
It is known that increased sympathetic nerve activity in chronic kidney disease (CKD) progressively worsens kidney function and hypertension. We tested the hypothesis that total renal denervation contributes to reduce sympathetic activation to different beds and improves renal function in 5/6 nephrectomy model of CKD in male Wistar rats. After eight weeks of 5/6 nephrectomy surgery there was an increase in mean arterial pressure (CKD 179±22mmHg, n=6 vs. control animals 108±9; p<0.05, n=6) with no changes in heart rate (HR). Sympathetic nerve activity was increased at different levels to the remaining kidney, splanchnic and lumbar beds compared to control (CTL) group (CKD rSNA: 150±50, n=9 vs. CTL 96±15, n=9; CKD sSNA: 129±51, n=5 vs. CTL 34±14, n=6; CKD lSNA: 203±35, n=8 vs. CTL 146±21, spikes/s, n=7, p<0.05). Three weeks after total renal denervation (DNX) MAP was normalized in the CKD rats (124±19mmHg, n=5, p<0.05), with no change in HR. The lSNA was normalized (151±40, n=5, vs. CKD 203±35 spikes/s, n=8) and sSNA was decreased in 49% (64±34, n=5 vs. CKD 129±51 spikes/s, n=5, p<0.05). Renal function, assessed by creatinine plasma levels was improved after renal denervation (CKD 1.50±0.64, n=8; vs. CKD+DNX 0.82±0.22mg/mL, n=8, p<0.05). These findings demonstrate that renal nerves contribute to the maintenance of hypertension in CKD by increasing sympathoexcitation to other beds.
已知慢性肾脏病（CKD）中交感神经活动增加会逐渐加重肾功能损害和高血压。我们在雄性Wistar大鼠的5/6肾切除CKD模型中测试了以下假设：完全肾去神经支配有助于减少对不同部位的交感神经激活，并改善肾功能。在进行5/6肾切除手术后八周，平均动脉压升高（CKD组179±22mmHg，n = 6，对照组动物为108±9；p<0.05，n = 6），心率（HR）无变化。与对照组（CTL）相比，CKD组对剩余肾脏、内脏和腰部部位的交感神经活动在不同水平上均增加（CKD肾交感神经活动：150±50，n = 9，CTL组为96±15，n = 9；CKD内脏交感神经活动：129±51，n = 5，CTL组为34±14，n = 6；CKD腰部交感神经活动：203±35，n = 8，CTL组为146±21，单位：脉冲/秒，n = 7，p<0.05）。完全肾去神经支配（DNX）三周后，CKD大鼠的平均动脉压恢复正常（124±19mmHg，n = 5，p<0.05），心率无变化。腰部交感神经活动恢复正常（151±40，n = 5，CKD组为203±35脉冲/秒，n = 8），内脏交感神经活动降低了49%（64±34，n = 5，CKD组为129±51脉冲/秒，n = 5，p<0.05）。通过血浆肌酐水平评估的肾功能在肾去神经支配后得到改善（CKD组1.50±0.64，n = 8；CKD+DNX组0.82±0.22mg/mL，n = 8，p<0.05）。这些发现表明，肾神经通过增加对其他部位的交感神经兴奋，在CKD高血压的维持中起作用。
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