Kang Seong Su, Kim Soo Wan, Lee Jongun
Department of Physiology, Chonnam National University Medical School, Gwangju, Korea.
Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Electrolyte Blood Press. 2007 Dec;5(2):89-94. doi: 10.5049/EBP.2007.5.2.89. Epub 2007 Dec 31.
The present study was aimed at investigating the role of type II 11β-hydroxysteroid dehydrogenase (IIβ-HSD II) in the development of hypertension. Two-kidney, one-clip (2K1C), deoxycorticosterone acetate (DOCA)/salt, or N (G)-nitro-L-arginine methyl ester (L-NAME) hypertension was induced in male Sprague-Dawley rats. Four weeks later, the expression of 11β-HSD II mRNA was determined in the kidney by Northern blot analysis. The plasma level of aldosterone was measured by radioimmunoassay. In 2K1C hypertension, the expression of 11β-HSD II was decreased in the clipped kidney and increased in the non-clipped kidney. The expression was increased in the remnant kidney of DOCA/salt hypertension, while decreased in the kidneys of L-NAME hypertension. The plasma level of aldosterone was increased, decreased, and remained unchanged in 2K1C, DOCA/salt, and L-NAME hypertension, respectively. The down-regulation of 11β-HSD II may contribute to the sodium retention, thereby increasing the blood pressure in 2K1C and L-NAME hypertension. On the contrary, the up-regulation in DOCA/salt hypertension may play a compensatory role to dissipate the sodium retention.
本研究旨在探讨II型11β-羟基类固醇脱氢酶（IIβ-HSD II）在高血压发生发展中的作用。在雄性Sprague-Dawley大鼠中诱导产生二肾一夹（2K1C）、醋酸脱氧皮质酮（DOCA）/盐或N（G）-硝基-L-精氨酸甲酯（L-NAME）高血压模型。四周后，通过Northern印迹分析测定肾脏中11β-HSD II mRNA的表达。采用放射免疫分析法测定血浆醛固酮水平。在2K1C高血压模型中，夹闭侧肾脏中11β-HSD II的表达降低，未夹闭侧肾脏中表达增加。在DOCA/盐高血压模型的残余肾脏中表达增加，而在L-NAME高血压模型的肾脏中表达降低。在2K1C、DOCA/盐和L-NAME高血压模型中，血浆醛固酮水平分别升高、降低和保持不变。11β-HSD II的下调可能导致钠潴留，从而在2K1C和L-NAME高血压中升高血压。相反，DOCA/盐高血压中的上调可能起到代偿作用以消除钠潴留。
