Liu Y J, Nakagawa Y, Ohzeki T
Department of Pediatrics, Hamamatsu University School of Medicine, Japan.
Hypertension. 1998 Mar;31(3):885-9. doi: 10.1161/01.hyp.31.3.885.
The presence of 11beta-hydroxysteroid dehydrogenase (11beta-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 11beta-HSD isoforms in diabetes-related hypertension, we measured the mean systolic blood pressure and the 11beta-HSD activity and mRNA levels for both 11beta-HSD1 and 11beta-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 11beta-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 11beta-HSD1 activity and mRNA expression in diabetic rats. Insulin administered subcutaneously to diabetic rats for 2 weeks completely reversed the decrease in renal 11beta-HSD2 activity and gene expression and prevented the elevation in blood pressure in the diabetic rat. These results indicate that alteration of renal 11beta-HSD2 activity and gene expression may be primarily responsible for the changes in blood pressure of STZ-diabetic rats after early treatment with insulin.
肾脏中11β-羟基类固醇脱氢酶（11β-HSD）的活性被认为在调节糖皮质激素诱导的电解质平衡紊乱和血压控制方面具有重要作用。为了评估11β-HSD同工型在糖尿病相关高血压中的可能作用，我们测量了链脲佐菌素（STZ）诱导的糖尿病雌性大鼠肾脏中11β-HSD1和11β-HSD2的平均收缩压、11β-HSD活性及mRNA水平。注射STZ（65mg/kg）三周后，糖尿病大鼠的平均收缩压比正常大鼠升高了13.6%（P<0.01）。糖尿病大鼠肾脏中的11β-HSD2活性及mRNA表达水平显著降低（P<0.01）。然而，STZ处理并未降低糖尿病大鼠肾脏中11β-HSD1的活性及mRNA表达水平。对糖尿病大鼠皮下注射胰岛素两周可完全逆转肾脏中11β-HSD2活性及基因表达的降低，并防止糖尿病大鼠血压升高。这些结果表明，肾脏中11β-HSD2活性及基因表达的改变可能是早期胰岛素治疗后STZ糖尿病大鼠血压变化的主要原因。
