Takeda Yoshiyu
Molecular Genetics of Cardiovascular Disorders, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Mol Cell Endocrinol. 2004 Mar 31;217(1-2):75-9. doi: 10.1016/j.mce.2003.10.012.
The author showed direct evidence that blood vessels are aldosteronogenic. The expression of CYP11B2 mRNA and synthesis of vascular aldosterone were decreased in rats treated with angiotensin converting enzyme inhibitor. Angiotensin II increased production of aldosterone in blood vessels. Vascular aldosterone and CYP11B2 mRNA levels of 2-week-old SHRSPs were significantly increased compared with that in WKY rats of the same age. High sodium intake develops and accelerates vascular injury and cardiac hypertrophy in SHRSP. Plasma aldosterone concentrations and plasma renin concentration were decreased by high salt intake in SHRSP. Aldosterone production, the expression of CYP11B2 mRNA and type I angiotensin II receptor (ATiR) mRNA in blood vessels were significantly increased by high salt intake. These results suggest that high salt intake increases aldosterone production and expression of the ATiR mRNA in the vascular tissue in SHRSP, which may contribute to the development of malignant hypertension in salt-loaded SHRSP.
作者展示了血管具有醛固酮生成作用的直接证据。用血管紧张素转换酶抑制剂处理的大鼠中，CYP11B2 mRNA的表达和血管醛固酮的合成减少。血管紧张素II增加血管中醛固酮的生成。与同龄WKY大鼠相比，2周龄SHRSPs的血管醛固酮和CYP11B2 mRNA水平显著升高。高钠摄入会发展并加速SHRSPs的血管损伤和心脏肥大。高盐摄入使SHRSPs的血浆醛固酮浓度和血浆肾素浓度降低。高盐摄入使血管中的醛固酮生成、CYP11B2 mRNA的表达以及I型血管紧张素II受体（ATiR）mRNA显著增加。这些结果表明，高盐摄入会增加SHRSPs血管组织中醛固酮的生成和ATiR mRNA的表达，这可能有助于盐负荷SHRSPs中恶性高血压的发展。
