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骨形态发生蛋白-6在肾上腺皮质细胞醛固酮调节中的作用。

Roles of bone morphogenetic protein-6 in aldosterone regulation by adrenocortical cells.

作者信息

Otani Hiroyuki, Otsuka Fumio, Inagaki Kenichi, Suzuki Jiro, Makino Hirofumi

机构信息

Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Detistry and Pharmaceucial Sciences, Okayama 700-8558, Japan.

出版信息

Acta Med Okayama. 2010 Aug;64(4):213-8. doi: 10.18926/AMO/40128.

Abstract

Aldosterone production occurs in the adrenal cortex, and is regulated primarily by angiotensin II (Ang II), potassium and adrenocorticotropin (ACTH). In the presence of the aldosterone stimulators, steroidogenesis is further governed by local autocrine and/or paracrine factors in the adrenal cortex. We reported the presence of functional bone morphogenetic protein (BMP) system in the adrenal cortex and also demonstrated that BMP-6 increases Ang II-induced aldosterone production, which could be involved in the "aldosterone breakthrough" phenomenon. Aldosterone breakthrough is the phenomenon by which circulating aldosterone concentrations increase above pre-treatment levels after long-term therapy with ACE inhibitors or Ang II type 1 receptor antagonists (ARB). This phenomenon may lead to important clinical consequences since increased aldosterone in a high-salt state facilitates cardiovascular and renal damage in hypertensive patients. We found that long-term ARB treatment reverses the reduction of aldosterone synthesis by adrenocortical cells, thereby causing "cellular aldosterone breakthrough". The availability of BMP-6 in the adrenal cortex may be at least partly involved in the occurrence of cellular escape from aldosterone suppression under chronic treatment with ARB.

摘要

醛固酮在肾上腺皮质中产生,主要受血管紧张素II(Ang II)、钾和促肾上腺皮质激素(ACTH)调节。在存在醛固酮刺激物的情况下,肾上腺皮质中的类固醇生成还受局部自分泌和/或旁分泌因子的进一步调控。我们报道了肾上腺皮质中存在功能性骨形态发生蛋白(BMP)系统,并且还证明BMP-6可增加Ang II诱导的醛固酮生成,这可能与“醛固酮突破”现象有关。醛固酮突破是指在长期使用血管紧张素转换酶抑制剂(ACEI)或1型血管紧张素II受体拮抗剂(ARB)治疗后,循环醛固酮浓度升高至治疗前水平以上的现象。这种现象可能会导致重要的临床后果,因为高盐状态下醛固酮增加会促进高血压患者的心血管和肾脏损害。我们发现长期使用ARB治疗可逆转肾上腺皮质细胞醛固酮合成的减少,从而导致“细胞醛固酮突破”。肾上腺皮质中BMP-6的存在可能至少部分参与了在ARB长期治疗下细胞逃避醛固酮抑制的发生。

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