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与血压变化相关的调节钠排泄的肾内机制。

Intrarenal mechanisms that regulate sodium excretion in relationship to changes in blood pressure.

作者信息

Romero J C, Bentley M D, Vanhoutte P M, Knox F G

机构信息

Department of Physiology and Biophysics.

出版信息

Mayo Clin Proc. 1989 Nov;64(11):1406-24. doi: 10.1016/s0025-6196(12)65383-x.

Abstract

Because pressure-related natriuresis may be central to the regulatory role of the kidney on blood pressure, it is important to understand the relationship of humoral systems involved in the control of renal hemodynamics and tubular function. The preglomerular endothelial synthesis of prostaglandin I2 and endothelium-derived relaxing factor seem to modulate autoregulatory control by the afferent arterioles and the release of renin by the juxtaglomerular apparatus. The release of renin is followed by an increase in angiotensin II in the renal interstitium, which is responsible for adjusting the vascular tone of the efferent arterioles and vasa recta and for stimulating proximal tubular reabsorption of sodium. Variations in medullary circulation induced by angiotensin II could alter medullary interstitial pressure and the medullary production of prostaglandins E2 and I2 and, ultimately, could modulate sodium reabsorption in the medullary thick ascending limbs and the collecting ducts.

摘要

由于压力相关性利钠作用可能是肾脏对血压调节作用的核心,因此了解参与肾血流动力学和肾小管功能控制的体液系统之间的关系非常重要。肾小球前内皮细胞合成前列腺素I2和内皮衍生舒张因子似乎可调节入球小动脉的自身调节控制以及球旁器释放肾素。肾素释放后,肾间质中血管紧张素II增加,这负责调节出球小动脉和直小血管的血管张力,并刺激近端肾小管对钠的重吸收。血管紧张素II引起的髓质循环变化可改变髓质间质压力以及前列腺素E2和I2的髓质生成,并最终调节髓质厚壁升支和集合管中的钠重吸收。

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