Cardiovascular Division, Department of Physiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil; Medical School, Universidade Municipal de São Caetano do Sul, São Paulo, Brazil; Instituto do Coração, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Cardiovascular Division, Department of Physiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.
Life Sci. 2021 Aug 1;278:119534. doi: 10.1016/j.lfs.2021.119534. Epub 2021 Apr 29.
Diabetes promotes renal sympathetic hyperactivity, autonomic imbalance, and cardiovascular and renal dysfunction. Bilateral renal denervation (BRD) has emerged as a treatment for diabetes; however, the mechanisms that underlie the beneficial effects of BRD are unknown.
The present study evaluated the effects of BRD on autonomic, cardiovascular, metabolic, and renal function in streptozotocin-diabetic rats.
Wistar rats were separated into three experimental groups: control (CTR), diabetic (DM), and diabetic that underwent BRD (DM BRD). BRD was performed two weeks after STZ-diabetes induction, the experiments were performed four weeks after DM induction. This study evaluated sympathetic vasomotor nerve activity in different territories (renal, lumbar and splanchnic), arterial baroreceptor reflex, metabolic and renal function.
BRD significantly reduced glycemia, glycosuria, albuminuria, and SGLT2 gene expression in the kidney in DM rats. Renal sympathetic nerve activity (rSNA) was significantly increased and splanchnic sympathetic nerve activity (sSNA) was significantly decreased in DM rats, without changes in lumbar sympathetic nerve activity (lSNA). BRD was able to normalize sSNA and significantly increase lSNA in DM rats compared to control rats. Additionally, cardiac baroreceptor sensitivity was impaired in DM rats, and BRD significantly improved baroreflex sensitivity.
Our data suggest that renal nerves play an important role in autonomic, cardiovascular, and renal dysfunction in STZ-DM rats. Thus, sympathetic renal hyperactivity should be considered a possible therapeutic target in diabetic patients.
本研究旨在评估去肾交感神经术（BRD）对链脲佐菌素诱导的糖尿病大鼠自主神经、心血管、代谢和肾功能的影响。
Wistar 大鼠分为三组：对照组（CTR）、糖尿病组（DM）和糖尿病去肾交感神经组（DM BRD）。BRD 在 STZ 诱导糖尿病后两周进行，实验在 DM 诱导后四周进行。本研究评估了不同区域（肾、腰和内脏）的交感血管运动神经活性、动脉压力感受器反射、代谢和肾功能。
BRD 可显著降低 DM 大鼠的血糖、糖尿、蛋白尿和肾脏 SGLT2 基因表达。DM 大鼠的肾交感神经活性（rSNA）显著增加，内脏交感神经活性（sSNA）显著降低，而腰交感神经活性（lSNA）无变化。与对照组相比，BRD 可使 DM 大鼠的 sSNA 正常化，并显著增加 lSNA。此外，DM 大鼠的心脏压力感受器敏感性受损，BRD 可显著改善压力反射敏感性。
我们的数据表明，肾脏神经在 STZ-DM 大鼠的自主神经、心血管和肾功能障碍中起重要作用。因此，交感神经肾活性亢进可能是糖尿病患者的一个潜在治疗靶点。
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