Maeda T, Furukawa I, Suzuki T, Mori H
Department of Pathology, Osaka Medical College, Japan.
Nephron. 1990;55(2):181-6. doi: 10.1159/000185949.
Intense proteinuria in rats bearing a functioning pituitary tumor MtT SA5 was considered to be evoked by overproduction of albumin due to elevated serum growth hormone (GH). The present study revealed a striking reduction of proteinuria by bilateral adrenalectomy. Supplementation for about 6 weeks with glucocorticoids to adrenalectomized tumor-bearing rats again induced marked proteinuria, but supplementation with mineralocorticoids failed to augment proteinuria. An analysis of systemic blood pressure and renal blood flow did not yield any conclusive result. In spite of an assumption that glucocorticoids enhance GH production of the tumor based on the presence of glucocorticoid receptor in the tumor tissue, no difference was found in serum GH levels between glucocorticoid- and mineralocorticoid-supplemented adrenalectomized rats. The mechanism remains to be clarified, but modification of glomerular permeability or a change in glomerular hydraulic pressure by glucocorticoids might be considered.
患有功能性垂体瘤MtT SA5的大鼠出现严重蛋白尿,被认为是由于血清生长激素(GH)升高导致白蛋白过度产生所致。本研究显示,双侧肾上腺切除术后蛋白尿显著减少。给肾上腺切除的荷瘤大鼠补充糖皮质激素约6周后,再次诱导出明显的蛋白尿,但补充盐皮质激素未能增加蛋白尿。对全身血压和肾血流量的分析未得出任何确定性结果。尽管基于肿瘤组织中存在糖皮质激素受体这一情况假设糖皮质激素会增强肿瘤的GH产生,但在补充糖皮质激素和盐皮质激素的肾上腺切除大鼠之间,血清GH水平未发现差异。其机制仍有待阐明,但可能考虑糖皮质激素对肾小球通透性的改变或肾小球液压的变化。