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首页> 外文期刊>Cell metabolism >Interleukin-1 Receptor Activation Potentiates Salt Reabsorption in Angiotensin II-Induced Hypertension via the NKCC2 Co-transporter in the Nephron
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Interleukin-1 Receptor Activation Potentiates Salt Reabsorption in Angiotensin II-Induced Hypertension via the NKCC2 Co-transporter in the Nephron

机译：白介素1受体激活通过肾单位中的NKCC2共转运蛋白增强血管紧张素II诱导的高血压中的盐重吸收。

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摘要

Hypertension is among the most prevalent and catastrophic chronic diseases worldwide. While the efficacy of renin angiotensin system (RAS) blockade in lowering blood pressure illustrates that the RAS is broadly activated in human hypertension, the frequent failure of RAS inhibition to prevent or reverse hypertensive organ damage highlights the need for novel therapies to combat RAS-dependent hypertension. We previously discovered elevated levels of the macrophage cytokine IL-1 in the kidney in a murine model of RAS-mediated hypertension. Here we report that IL-1 receptor (IL-1R1) deficiency or blockade limits blood pressure elevation in this model by mitigating sodium reabsorption via the NKCC2 co-transporter in the nephron. In this setting, IL-1R1 activation prevents intra-renal myeloid cells from maturing into Ly6C(+)Ly6G(-) macrophages that elaborate nitric oxide, a natriuretic hormone that suppresses NKCC2 activity. By revealing how the innate immune system regulates tubular sodium transport, these experiments should lead to new immunomodulatory anti-hypertensive therapies.
机译：高血压是全世界最流行和灾难性的慢性疾病之一。肾素血管紧张素系统（RAS）降低血压的功效说明RAS在人类高血压中被广泛激活，但RAS抑制的频繁失败阻止了预防或逆转高血压器官损害，这凸显出需要新的疗法来对抗RAS依赖性高血压。我们先前在RAS介导的高血压鼠模型中发现肾脏中巨噬细胞细胞因子IL-1的水平升高。在这里，我们报道IL-1受体（IL-1R1）缺乏或受阻，通过减轻肾单位中NKCC2共同转运蛋白钠的重吸收，限制了该模型的血压升高。在这种情况下，IL-1R1激活可防止肾内髓样细胞成熟为精制一氧化氮（一种抑制NKCC2活性的利钠激素）的Ly6C（+）Ly6G（-）巨噬细胞。通过揭示先天免疫系统如何调节肾小管钠转运，这些实验应导致新的免疫调节抗高血压疗法。

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