Mineralocorticoid modulation of rabbit medullary collecting duct acidification. A sodium-independent effect.
Mineralocorticoid modulation of rabbit medullary collecting duct acidification. A sodium-independent effect.
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盐皮质激素调节兔髓质集合管酸化。
DOI：
10.1172/jci110986
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Jacobson,HR
中科院分区：
文献类型：
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作者：
Stone,DK;Seldin,DW;Kokko,JP;Jacobson,HR
来自外髓质内条纹的兔髓质集合管（MCD）已被确定为主要的远端肾单位酸化位点。分离的灌注小管技术用于检查盐皮质激素和糖皮质激素在 MCD 酸化调节中的作用。肾上腺切除术将碳酸氢盐重吸收率（JHCO3，pmol X mm-1 X min-1）从正常值 9.79 +/- 1.21 降低至 0.67 +/- 1.1。长期给予醋酸脱氧皮质酮 (DOCA) 显着增加 MCD 的 JHCO3 至 18.02 +/- 1.62，而长期给予地塞米松不影响 JHCO3。醛固酮和地塞米松对 MCD 酸化的直接影响通过在醛固酮或地塞米松存在下灌注从肾上腺切除的兔子收获的小管来检查。 5 X 10(-8) M 醛固酮使 JHCO3 从 1.27 +/- 0.28 显着增加至 3.09 +/- 0.34。在 10(-6) M 时，醛固酮使 JHCO3 产生更大的增加，从 0.67 +/- 1.1 增加到 9.39 +/- 1.59。体外地塞米松治疗对 JHCO3 没有影响。检查醛固酮刺激酸化的钠依赖性的研究表明，从正常动物和醋酸脱氧皮质酮处理的动物中收获的肾小管中的 JHCO3 不受四甲基铵完全替代钠的影响。同样，鲁米那阿米洛利 (5 X 10(-5) M) 对肾上腺切除动物和正常动物的肾小管中的 JHCO3 没有影响。此外，醛固酮的急性体外刺激作用被发现在鲁米那阿米洛利存在的情况下发生。这些研究定义了哺乳动物远端肾单位段具有主要的酸化能力，该能力受盐皮质激素调节，但与管腔钠无关。
Rabbit medullary collecting duct (MCD) from inner stripe of outer medulla has been identified as a major distal nephron acidification site. The isolated, perfused tubule technique was used to examine the roles of mineralocorticoid and glucocorticoid in regulation of MCD acidification. Surgical adrenalectomy reduced bicarbonate reabsorptive rate (JHCO3, pmol X mm-1 X min-1) from the normal of 9.79 +/- 1.21 to 0.67 +/- 1.1. Chronic administration of deoxycorticosterone acetate (DOCA) increased JHCO3 of MCD significantly to 18.02 +/- 1.62 whereas chronic dexamethasone administration did not affect JHCO3. The direct effects of aldosterone and dexamethasone upon MCD acidification were examined by perfusing tubules harvested from adrenalectomized rabbits in the presence of aldosterone or dexamethasone. Aldosterone, at 5 X 10(-8) M, increased JHCO3 significantly from 1.27 +/- 0.28 to 3.09 +/- 0.34. At 10(-6) M, aldosterone produced a greater increase in JHCO3 from 0.67 +/- 1.1 to 9.39 +/- 1.59. In vitro dexamethasone treatment had no effect on JHCO3. Studies examining the sodium dependence of aldosterone-stimulated acidification demonstrated that JHCO3 in tubules harvested from normal and deoxycorticosterone acetate-treated animals was unaffected by total replacement of sodium with tetramethylammonium. Likewise, luminal amiloride (5 X 10(-5) M) had no effect on JHCO3 in tubules harvested from adrenalectomized and normal animals. Moreover, the acute, in vitro stimulatory effect of aldosterone was seen to occur in the presence of luminal amiloride. These studies define a mammalian distal nephron segment that possesses major acidifying capacity, which is modulated by mineralocorticoid but independent of luminal sodium.