3. Vascular aldosterone. Biosynthesis and a link to angiotensin II-induced hypertrophy of vascular smooth muscle cells
3. Vascular aldosterone. Biosynthesis and a link to angiotensin II-induced hypertrophy of vascular smooth muscle cells
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3.血管醛固酮。
DOI：
10.1007/bf03349773
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发表时间：
1994
影响因子：
5.4
通讯作者：
E. Gomez
中科院分区：
文献类型：
--
作者：
H. Hatakeyama;I. Miyamori;T. Fujita;Y. Takeda;R. Takeda;H. Yamamoto;E. Gomez
盐皮质激素被认为作用于血管，导致血管反应性和外周阻力增加。然而，到目前为止，它们的产生部位被认为只是肾上腺皮质。在这里，我们显示直接的证据表明，血管细胞本身是醛固酮，拥有自己的系统，响应类固醇。应用逆转录聚合酶链反应技术，在培养的人肺动脉内皮细胞和平滑肌细胞中检测到编码醛固酮生物合成关键酶的CYP 11 B2 mRNA。醛固酮受体（1型盐皮质激素受体）基因也被发现在平滑肌细胞中表达，在较小程度上，在内皮细胞中。血管紧张素II（肾素-血管紧张素系统的效应肽）刺激平滑肌细胞中的CYP 11B 2基因表达。此外，血管紧张素II诱导的[3 H]亮氨酸掺入平滑肌细胞的增加显着增强醛固酮，但抑制ZK 91587，1型盐皮质激素受体拮抗剂。这可能表明血管醛固酮参与了血管紧张素II诱导的血管平滑肌细胞肥大。因此，本研究提供了一个新的理解血管重塑和高血压的分子基础的起点。
Mineralocorticoids have been suggested to act on blood vessels, leading to increased vasoreactivity and peripheral resistance. However, the site of their production has so far been believed to be only the adrenal cortex. Here, we show direct evidence that vascular cells per se are aldosteronogenic, possessing their own system that responds to the steroid. Using polymerase chain reaction after reverse transcription, the CYP11B2 mRNA encoding the key enzyme for the biosynthesis of aldosterone was detected in both endothelial cells and smooth muscle cells cultivated from human pulmonary artery. The aldosterone receptor (type 1 mineralocorticoid receptor) gene was also found to be expressed in smooth muscle cells and, to a lesser extent, in endothelial cells. CYP11B2 gene expression in smooth muscle cells was stimulated by angiotensin II, the effector peptide of the renin-angiotensin system. Furthermore, the angiotensin II-induced increase in [3H]leucine incorporation in smooth muscle cells was significantly enhanced by aldosterone but inhibited by ZK 91587, a type 1 mineralocorticoid receptor antagonist. This may indicate that vascular aldosterone participates in the angiotensin II-induced hypertrophy of vascular smooth muscle cells. The present study therefore provides the starting point for a novel understanding of the molecular basis of vascular remodeling and hypertension.