Rubattu S, Russo R, Gigante B, Porcellini A, Finizia L, Trimarco B, Volpe M
Department of Internal Medicine, Federico II University, Naples, Italy.
J Hypertens. 1995 Nov;13(11):1253-8. doi: 10.1097/00004872-199511000-00006.
To investigate whether hypercholesterolaemia interferes with the expression of the enzymes involved in steroid biosynthesis in the adrenal cortex.
Twenty-four 5-week-old male spontaneously hypertensive rats (SHR) were randomly assigned to a high (1%) cholesterol diet (n = 8) or to a matched cholesterol-free diet (n = 8) for 6 weeks. A third group (n = 8) was studied after 2 weeks of washout from the high-cholesterol intake. A cohort of age- and sex-matched normotensive Wistar-Kyoto (WKY) rats (n = 24) underwent the same treatments and was used as a control.
In SHR cholesterol feeding reduced urinary sodium excretion (0.8 +/- 0.1 versus 1.4 +/- 0.1 mmol/24 h in the cholesterol-free group), increased plasma aldosterone levels (299 +/- 60 versus 154 +/- 24) and reduced plasma corticosterone levels (142 +/- 21 versus 278 +/- 35 ng/ml). Those responses were associated with a reduction of 11 beta-hydroxylase cytochrome P450 messenger RNA (mRNA) in the adrenal cortex (-52.3 +/- 3.4%) whereas aldosterone synthase mRNA remained unchanged. That effect and the changes in electrolyte excretion and steroid levels were no longer detectable after withdrawal of the diet. In WKY rats high-cholesterol diet induced no significant changes in urinary electrolyte excretion, steroid levels and expression of 11 beta-hydroxylase cytochrome P450 and aldosterone synthase in the adrenals.
The present results indicate that in SHR hypercholesterolaemia selectively interferes with the adrenal steroid biosynthetic pathway by reducing the expression of 11 beta-hydroxylase, leading to accumulation of mineralocorticoids and sodium retention.
研究高胆固醇血症是否会干扰肾上腺皮质中参与类固醇生物合成的酶的表达。
将24只5周龄雄性自发性高血压大鼠(SHR)随机分为两组,一组给予高胆固醇饮食(1%,n = 8),另一组给予匹配的无胆固醇饮食(n = 8),持续6周。第三组(n = 8)在高胆固醇饮食摄入2周后洗脱2周进行研究。选取一组年龄和性别匹配的正常血压Wistar-Kyoto(WKY)大鼠(n = 24)进行相同处理并作为对照。
在SHR中,胆固醇喂养降低了尿钠排泄(无胆固醇组为1.4±0.1 mmol/24 h,胆固醇喂养组为0.8±0.1 mmol/24 h),增加了血浆醛固酮水平(分别为299±60和154±24),并降低了血浆皮质酮水平(分别为142±21和278±35 ng/ml)。这些反应与肾上腺皮质中11β-羟化酶细胞色素P450信使核糖核酸(mRNA)减少(-52.3±3.4%)相关,而醛固酮合酶mRNA保持不变。停止饮食后,这种效应以及电解质排泄和类固醇水平的变化不再能检测到。在WKY大鼠中,高胆固醇饮食未引起尿电解质排泄、类固醇水平以及肾上腺中11β-羟化酶细胞色素P450和醛固酮合酶表达的显著变化。
目前的结果表明,在SHR中,高胆固醇血症通过降低11β-羟化酶的表达选择性地干扰肾上腺类固醇生物合成途径,导致盐皮质激素蓄积和钠潴留。