The Role of Interleukin-6 in Regulating Glomerular Filtration Rate during Angiotensin II and High Salt Conditions

IF 5.3 2区 医学 Q1 PHYSIOLOGY Physiology Pub Date : 2024-05-01 DOI:10.1152/physiol.2024.39.s1.1923
Mark Hatcher, Rong Duan, Dexter Lee
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Abstract

Previous results demonstrate that interleukin-6 (IL-6) increases mean arterial pressure (MAP) during Angiotensin II (Ang II)-salt hypertension. In addition, albumin excretion was lower in IL-6 knockout mice (KO) when compared to wild-type (WT). This study investigated the role of IL-6 on regulating glomerular filtration rate (GFR), renal plasma flow (RPF) and MAP in WT and IL-6 KO mice treated with a slow pressor dose of Ang II (200 ng/kg/min) +/- 6% high-salt (HS) diet. Male C57BL6 and IL-6 KO mice (12 weeks old) were treated with Ang II +/- 6% HS diet for 12 – 14 days. Mean arterial pressure, RPF and GFR were measured in anesthetized mice. MAP was 130 ± 7 mmHg and 91 ± 4 mmHg in control WT and IL-6 KO mice, respectively. Ang II treatment increased MAP in WT (153 ± 5 mmHg) and no change in IL-6 KO (83 ± 4 mmHg) mice. Ang II + 6% HS increased MAP to 150 ± 11 mmHg in WT and 93 ± 4 mmHg in IL-6 KO mice. Baseline RPF was 1822 ± 229 and 1912 ± 402 ml/min/g in control WT and IL-6 KO mice, respectively. Ang II treatment increased RPF in WT (3156 ± 753 ml/min/g), while lowering RPF in IL-6 KO (1648 ± 422 ml/min/g) mice. RPF during Ang II + 6% HS treatment was decreased in WT (1095 ± 305 ml/min/g) and IL-6 KO (1133 ml/min/g) mice. GFR was 756 ± ml/min/g and 788 ± ml/min/g in control WT and IL-6 KO mice, respectively. Ang II increased GFR in WT (1009 ± 63 ml/min/g) and no change in IL-6 KO (756 ± 23 ml/min/g). Ang II + 6% HS increased GFR in WT (1095 ± 146 ml/min/g) and no change in GFR of IL-6 KO (540 ± 207 ml/min/g) mice. Our results suggest that IL-6 reduces MAP during baseline, Ang II, and Ang II + 6% HS. The absence of IL-6 prevented increases in MAP, RPF and GFR during Ang II treatment. Our data also suggest that IL-6 contributes to increased MAP and GFR during Ang II + 6% HS treatment. K01HL092593-05. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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白细胞介素-6 在血管紧张素 II 和高盐条件下调节肾小球滤过率的作用
之前的研究结果表明,白细胞介素-6(IL-6)会在血管紧张素II(Ang II)-盐高血压期间增加平均动脉压(MAP)。此外,与野生型(WT)相比,IL-6基因敲除小鼠(KO)的白蛋白排泄量较低。本研究调查了IL-6对WT和IL-6 KO小鼠肾小球滤过率(GFR)、肾血浆流量(RPF)和MAP的调节作用,WT和IL-6 KO小鼠接受缓慢加压剂量的Ang II(200纳克/千克/分钟)+/- 6%高盐(HS)饮食。雄性 C57BL6 和 IL-6 KO 小鼠(12 周大)接受 Ang II +/- 6% HS 饮食治疗 12 - 14 天。在麻醉状态下测量小鼠的平均动脉压、RPF 和 GFR。对照组 WT 小鼠和 IL-6 KO 小鼠的 MAP 分别为 130 ± 7 mmHg 和 91 ± 4 mmHg。Ang II治疗可提高WT小鼠的MAP(153 ± 5 mmHg),而IL-6 KO小鼠的MAP没有变化(83 ± 4 mmHg)。Ang II + 6% HS 可使 WT 小鼠的 MAP 增至 150 ± 11 mmHg,IL-6 KO 小鼠的 MAP 增至 93 ± 4 mmHg。对照组 WT 小鼠和 IL-6 KO 小鼠的基线 RPF 分别为 1822 ± 229 和 1912 ± 402 ml/min/g。Ang II 治疗可增加 WT 小鼠的 RPF(3156 ± 753 毫升/分钟/克),而降低 IL-6 KO 小鼠的 RPF(1648 ± 422 毫升/分钟/克)。WT 小鼠(1095 ± 305 毫升/分钟/克)和 IL-6 KO 小鼠(1133 毫升/分钟/克)在 Ang II + 6% HS 治疗期间的 RPF 均下降。对照组 WT 小鼠和 IL-6 KO 小鼠的 GFR 分别为 756 ± ml/min/g 和 788 ± ml/min/g。Ang II 可增加 WT 小鼠的 GFR(1009 ± 63 ml/min/g),而 IL-6 KO 小鼠的 GFR 无变化(756 ± 23 ml/min/g)。Ang II + 6% HS 可增加 WT 小鼠的 GFR(1095 ± 146 毫升/分钟/克),而 IL-6 KO 小鼠的 GFR(540 ± 207 毫升/分钟/克)无变化。我们的结果表明,IL-6 可降低基线、Ang II 和 Ang II + 6% HS 期间的 MAP。缺失 IL-6 可防止 Ang II 治疗期间 MAP、RPF 和 GFR 的增加。我们的数据还表明,在 Ang II + 6% HS 治疗期间,IL-6 有助于增加 MAP 和 GFR。K01HL092593-05。本文是在 2024 年美国生理学峰会上发表的摘要全文,仅提供 HTML 格式。本摘要没有附加版本或附加内容。生理学》未参与同行评审过程。
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来源期刊
Physiology
Physiology 医学-生理学
CiteScore
14.50
自引率
0.00%
发文量
37
期刊介绍: Physiology journal features meticulously crafted review articles penned by esteemed leaders in their respective fields. These articles undergo rigorous peer review and showcase the forefront of cutting-edge advances across various domains of physiology. Our Editorial Board, comprised of distinguished leaders in the broad spectrum of physiology, convenes annually to deliberate and recommend pioneering topics for review articles, as well as select the most suitable scientists to author these articles. Join us in exploring the forefront of physiological research and innovation.
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