Suzuki S, Tsubochi H, Suzuki T, Darnel A D, Krozowski Z S, Sasano H, Kondo T
Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Exp Lung Res. 2001 Mar;27(2):143-55. doi: 10.1080/019021401750069384.
We examined whether transalveolar fluid transport is modulated by aldosterone in adult rats. Because colocalization of mineralocorticoid receptors (MR) with 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) is important for aldosterone specific action, we first determined the immunohistochemical distribution of MR and 11betaHSD2 in the lung. We found that alveolar epithelial cells express both MR and 11betaHSD2. Reverse transcriptase polymerase chain reaction (RT-PCR) demonstrated that rat alveolar type II epithelial cells express both MR and 11betaHSD2. We then measured alveolar fluid clearance in rats treated with chronic low-sodium diet. A low-sodium diet (0.1% NaCl for 12 to 14 days) caused hyperaldosteronism accompanied by hypokalemia, whereas serum corticosterone and adrenaline levels remained normal. We found that hyperaldosteronism was associated with significantly higher alveolar fluid clearance and that this increase was related to the amiloride-sensitive component. In addition, the increase in alveolar fluid clearance was inhibited by spironolactone. Our results show that aldosterone is able to stimulate Na+ channels of alveolar epithelial cells. We conclude that alveolar epithelium is a physiological target tissue for aldosterone and transalveolar fluid absorption could in part be modulated by endogenous aldosterone acting via MR.
我们研究了成年大鼠经肺泡的液体转运是否受醛固酮调节。由于盐皮质激素受体（MR）与2型11β-羟基类固醇脱氢酶（11βHSD2）的共定位对醛固酮的特异性作用很重要，我们首先确定了MR和11βHSD2在肺中的免疫组织化学分布。我们发现肺泡上皮细胞同时表达MR和11βHSD2。逆转录聚合酶链反应（RT-PCR）表明大鼠II型肺泡上皮细胞同时表达MR和11βHSD2。然后我们测量了用慢性低钠饮食处理的大鼠的肺泡液体清除率。低钠饮食（0.1%氯化钠，持续12至14天）导致醛固酮增多症并伴有低钾血症，而血清皮质酮和肾上腺素水平保持正常。我们发现醛固酮增多症与显著更高的肺泡液体清除率相关，并且这种增加与氨氯地平敏感成分有关。此外，肺泡液体清除率的增加受到螺内酯的抑制。我们的结果表明醛固酮能够刺激肺泡上皮细胞的钠通道。我们得出结论，肺泡上皮是醛固酮的生理靶组织，经肺泡的液体吸收可能部分受内源性醛固酮通过MR起作用的调节。
