Mechanism of prostasin-induced aldosterone production

血压（BP）和细胞外液量的控制主要取决于肾脏对钠重吸收和排泄的调节。上皮钠通道（ENaC）通过调节肾脏中的钠重吸收而在血压调节中起重要作用。我们以前发现，前列腺素增加钠运输通过ENaC在共表达系统中使用非洲爪蟾卵母细胞，和醛固酮增加了丰富的前列腺素在人类和大鼠尿液和小鼠皮质集合管细胞系的培养基中，我们检查，如果前列腺素增加醛固酮合成在人类肾上腺皮质细胞系（H295R细胞）。使用CYP11B2启动子的荧光素酶测定用于观察前列腺素是否增加CYP11B2的转录活性。此外，在盐敏感性高血压的模型动物Dahl高血压大鼠中研究ENaC活性。

The control of blood pressure (BP) and extracellular fluid volume primarily depends on renal regulation of sodium reabsorption and excretion. The epithelial sodium channel (ENaC) plays an important role in the regulation of blood pressure by modulating Na reabsorption in the kidney. We previously revealed that prostasin increased Na transport through ENaC in the co-expression system using Xenopus oocytes, and that aldosterone increased the abundance of prostasin in human and rat urine and in the cultured medium of a mouse cortical collecting duct cell line.We examine if prostasin increases the aldosterone synthesis in a human adrenocortical cell line (H295R cells). Luciferase assay using CYP11B2 promoter is used to see if the prostasin increases the transcriptional activity of CYP11B2. In addition, ENaC activity is investigated in Dahl hypertensive rats which are the model animal of salt-sensitive hypertension.