Gene expression of 11β-hydroxysteroid dehydrogenase type 1 and type 2 in the kidneys of insulin-dependent diabetic rats

被引：18

作者：

Liu, YJ ^{[1
]}

Nakagawa, Y ^{[1
]}

Ohzeki, T ^{[1
]}

机构：

[1] Hamamatsu Univ Sch Med, Dept Pediat, Hamamatsu, Shizuoka 43131, Japan

来源：

HYPERTENSION | 1998年 / 31卷 / 03期

关键词：

11; beta-hydroxysteroid; dehydrogenase; streptozotocin; diabetes mellitus; kidney; blood pressure; insulin;

D O I：

10.1161/01.HYP.31.3.885

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

The presence of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) activity in the kidney has been suggested to be important in the regulation of glucocorticoid-induced disorders of electrolyte balance and the control of blood pressure. To assess the possible effect of 11 beta-HSD isoforms in diabetes-related hypertension, we measured the mean systolic blood pressure and the 11 beta-HSD activity and mRNA levels for both 11 beta-HSD1 and 11 beta-HSD2 in the kidney of streptozotocin (STZ)-diabetic female rats. Three weeks after injection of STZ (65 mg/kg), the mean systolic blood pressure of diabetic rats was elevated 13.6% above that of normal rats (P<.01). The renal 11 beta-HSD2 activity and level of mRNA expression were significantly decreased in diabetic rats (P<.01). However, the treatment of rats with STZ did not decrease the levels of renal 11 beta-HSD1 activity and mRNA expression in diabetic rats. insulin administered subcutaneously to diabetic rats for 2 weeks completely reversed the decrease in renal 11 beta-HSD2 activity and gene expression and prevented the elevation in blood pressure in the diabetic rat. These results indicate that alteration of renal 11 beta-HSD2 activity and gene expression may be primarily responsible for the changes in blood pressure of STZ-diabetic rats after early treatment with insulin.

引用

页码：885 / 889

页数：5

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