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首页> 外文期刊>American Journal of Physiology >Role of renal cortical cyclooxygenase-2 expression in hyperfiltration in rats with high-protein intake.
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Role of renal cortical cyclooxygenase-2 expression in hyperfiltration in rats with high-protein intake.

机译：肾皮质环氧合酶2表达在高蛋白摄入大鼠超滤中的作用。

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Renal cortical cyclooxygenase-2 (COX-2) is restricted to the macula densa and adjacent cortical thick ascending limbs (MD/cTALH). Renal cortical COX-2 increases in response to diabetes and renal ablation, both of which are characterized by hyperfiltration and reduced NaCl delivery to the MD due to increased proximal NaCl reabsorption. High-protein intake also induces hyperfiltration and decreases NaCl delivery to the MD due to increased NaCl reabsorption proximally. We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. Cortical COX-2 increased after protein loading but decreased after protein restriction. COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake.
机译：肾皮质环氧合酶2（COX-2）仅限于黄斑部和邻近的皮质粗大上升肢（MD / cTALH）。肾皮质COX-2响应于糖尿病和肾消融而增加，这两者的特征是超滤作用和由于近端NaCl重吸收增加而导致NaCl向MD的递送减少。由于近端NaCl的吸收增加，高蛋白摄入也会诱导超滤并减少NaCl输送至MD的速度。我们调查了高蛋白是否诱导皮质COX-2以及皮质COX-2是否有助于高蛋白诱导的超滤和肾内肾素生物合成的增加。皮质COX-2蛋白质加载后增加，但蛋白质限制后降低。 COX-2抑制减弱了高蛋白诱导的超滤，但对高蛋白诱导的肾内肾素升高没有影响。因此，诱导皮质COX-2促进了高蛋白诱导的超滤，但没有引起肾内肾素的升高。在肾皮质中，神经元一氧化氮合酶（nNOS）也定位于MD，并且已经提出了肾内nNOS与COX-2系统之间的相互作用。在盐限制中看到的皮质COX-2升高被nNOS抑制剂阻止。蛋白质加载后皮质nNOS表达也增加，并且对nNOS活性的抑制作用完全逆转了高蛋白诱导的皮质COX-2升高和超滤。这些结果表明，NO是高蛋白诱导的皮质COX-2升高的介体，并表明肾内nNOS和COX-2系统似乎都可以调节高蛋白摄入中所见的小动脉张力和随后的超滤。

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