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糖尿病中的肾脏交感神经活性通过 5-HT 受体激活通过 NO 通路调节。

Renal Sympathetic Hyperactivity in Diabetes Is Modulated by 5-HT Receptor Activation via NO Pathway.

机构信息

Laboratorio de Farmacología, Departamento de Fisiología y Farmacología, Facultad de Farmacia, Universidad de Salamanca, 37007 Salamanca, Spain.

Instituto de Investigación Biomédica de Salamanca (IBSAL), Paseo San Vicente 58-182, 37007 Salamanca, Spain.

出版信息

Int J Mol Sci. 2023 Jan 10;24(2):1378. doi: 10.3390/ijms24021378.

DOI:10.3390/ijms24021378
PMID:36674892
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9865738/
Abstract

Renal vasculature, which is highly innervated by sympathetic fibers, contributes to cardiovascular homeostasis. This renal sympathetic outflow is inhibited by 5-HT in normoglycaemic rats. Considering that diabetes induces cardiovascular complications, we aimed to determine whether diabetic state modifies noradrenergic input at renal level and its serotonergic modulation in rats. Alloxan diabetic rats were anaesthetized (pentobarbital; 60 mg/kg i.p.) and prepared for in situ autoperfusion of the left kidney to continuously measure systemic blood pressure (SBP), heart rate (HR), and renal perfusion pressure (RPP). Electrical stimulation of renal sympathetic outflow induces frequency-dependent increases (Δ) in RPP (23.9 ± 2.1, 59.5 ± 1.9, and 80.5 ± 3.5 mm Hg at 2, 4, and 6 Hz, respectively), which were higher than in normoglycaemic rats, without modifying HR or SBP. Intraarterial bolus of 5-HT and 5-CT (5-HT agonist) reduced electrically induced ΔRPP. Only L-694,247 (5-HT agonist) reproduced 5-CT inhibition on sympathetic-induced vasoconstrictions, whereas it did not modify exogenous noradrenaline-induced ΔRPP. 5-CT inhibition was exclusively abolished by i.v. bolus of LY310762 (5-HT antagonist). An inhibitor of guanylyl cyclase, ODQ (i.v.), completely reversed the L-694,247 inhibitory effect. In conclusion, diabetes induces an enhancement in sympathetic-induced vasopressor responses at the renal level. Prejunctional 5-HT receptors, via the nitric oxide pathway, inhibit noradrenergic-induced vasoconstrictions in diabetic rats.

摘要

肾脏血管系统受到交感神经纤维的高度支配，有助于心血管稳态。在正常血糖的大鼠中，5-HT 抑制肾交感神经输出。考虑到糖尿病会引起心血管并发症，我们旨在确定糖尿病状态是否改变了肾脏水平的去甲肾上腺素输入及其在大鼠中的 5-HT 调制。链脲佐菌素诱导的糖尿病大鼠用戊巴比妥（60mg/kg，ip）麻醉，并准备进行左肾原位自发灌注，以连续测量全身血压（SBP）、心率（HR）和肾灌注压（RPP）。肾交感神经输出的电刺激引起 RPP 的频率依赖性增加（Δ）（在 2、4 和 6 Hz 时分别为 23.9±2.1、59.5±1.9 和 80.5±3.5mmHg），高于正常血糖大鼠，而不改变 HR 或 SBP。动脉内注射 5-HT 和 5-CT（5-HT 激动剂）可减少电刺激引起的 ΔRPP。只有 L-694,247（5-HT 激动剂）重现了 5-CT 对交感神经诱导的血管收缩的抑制作用，而它没有改变外源性去甲肾上腺素引起的 ΔRPP。5-CT 抑制仅被静脉内注射 LY310762（5-HT 拮抗剂）所消除。鸟苷酸环化酶抑制剂 ODQ（静脉内）完全逆转了 L-694,247 的抑制作用。总之，糖尿病引起肾脏水平的交感神经诱导的血管加压反应增强。前突触 5-HT 受体通过一氧化氮途径抑制糖尿病大鼠中的去甲肾上腺素诱导的血管收缩。

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