血管紧张素-Ⅱ-1a 型受体 (AT1aR) 与隔夜低 Na+ 摄入时的肾 K+ 消耗。

IF 10.3 1区医学 Q1 UROLOGY & NEPHROLOGY

Journal of The American Society of Nephrology Pub Date : 2024-11-01 Epub Date: 2024-06-24 DOI:10.1681/ASN.0000000000000429

Xin-Peng Duan, Jun-Ya Zheng, Yu Xiao, Cheng-Biao Zhang, Dao-Hong Lin, Wen-Hui Wang

引用次数: 0

摘要

背景：慢性血管紧张素-II（Ang-II）灌注通过血管紧张素-II-1a型受体（AT1aR）刺激DCT的Kir4.1/Kir5.1，低钠摄入也刺激Kir4.1/Kir5.1。然而，目前尚未探究 AT1aR 在介导 LS 对 Kir4.1/Kir5.1 的影响中的作用：我们使用贴片钳技术检测了DCT的Kir4.1/Kir5.1活性，使用免疫印迹技术检测了NCC的表达/活性，并使用体内灌流技术测量了对照组、肾小管特异性AT1aR基因敲除小鼠（Ks-AT1aR-KO）和DCT特异性AT1aR基因敲除小鼠（DCT-AT1aR- KO）的肾脏Na+和肾脏K+-分泌：结果：Ang-II能急性刺激40-pS-K+通道（Kir4.1/Kir5.1-heterotetramer），增加全细胞Kir4.1/Kir5.1介导的K+电流和DCT-膜电位的负性，但只在晚期-DCT2中增加，而在早期-DCT中没有增加。急性 Ang-II 增加了噻嗪类药物诱导的肾脏 Na+ 排泄（ENa）。在 Ks-AT1aR-KO 小鼠中，Ang-II 对 Kir4.1/Kir5.1 和 HCTZ 诱导的 ENa 没有影响。在对照组小鼠中，隔夜低盐刺激了 DCT 中 Agtr1a mRNA 的表达，增加了晚期 DCT 中全细胞 Kir4.1/Kir5.1 介导的 K+ 电流，使晚期 DCT 膜超极化，增加了磷酸-Na-Cl-共转运体（pNCC）的表达，并增强了噻嗪类药物诱导的肾ENa。然而，隔夜低盐对 Kir4.1/Kir5.1 活性、DCT 膜电位和 NCC 活性/表达的影响在 DCT-AT1aR-KO 或 Ks-AT1aR-KO 小鼠中被取消。隔夜低盐对对照组小鼠的基线肾K+排泄（EK）和血浆K+浓度没有影响，但却增加了DCT-AT1aR-KO或Ks-AT1aR-KO小鼠的基线肾EK，降低了血浆K+浓度：急性 Ang-II 或隔夜低盐刺激晚期 DCT 的 Kir4.1/Kir5.1，AT1aR 是急性 Ang-II 或隔夜低盐诱导刺激 Kir4.1/Kir5.1 和 NCC 的原因。DCT的AT1aR在维持过夜-低盐期间足够的肾-EK基线和血浆K+浓度中发挥作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.

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来源期刊

Journal of The American Society of Nephrology 医学-泌尿学与肾脏学

CiteScore

22.40

自引率

2.90%

发文量

492

审稿时长

3-8 weeks

期刊介绍： The Journal of the American Society of Nephrology (JASN) stands as the preeminent kidney journal globally, offering an exceptional synthesis of cutting-edge basic research, clinical epidemiology, meta-analysis, and relevant editorial content. Representing a comprehensive resource, JASN encompasses clinical research, editorials distilling key findings, perspectives, and timely reviews. Editorials are skillfully crafted to elucidate the essential insights of the parent article, while JASN actively encourages the submission of Letters to the Editor discussing recently published articles. The reviews featured in JASN are consistently erudite and comprehensive, providing thorough coverage of respective fields. Since its inception in July 1990, JASN has been a monthly publication. JASN publishes original research reports and editorial content across a spectrum of basic and clinical science relevant to the broad discipline of nephrology. Topics covered include renal cell biology, developmental biology of the kidney, genetics of kidney disease, cell and transport physiology, hemodynamics and vascular regulation, mechanisms of blood pressure regulation, renal immunology, kidney pathology, pathophysiology of kidney diseases, nephrolithiasis, clinical nephrology (including dialysis and transplantation), and hypertension. Furthermore, articles addressing healthcare policy and care delivery issues relevant to nephrology are warmly welcomed.

血管紧张素-Ⅱ-1a 型受体 (AT1aR) 与隔夜低 Na+ 摄入时的肾 K+ 消 耗。

摘要

血管紧张素-Ⅱ-1a 型受体 (AT1aR) 与隔夜低 Na+ 摄入时的肾 K+ 消耗。