Spitzer A
Kidney Int. 1982 Apr;21(4):539-45. doi: 10.1038/ki.1982.60.
Evidence is presented that the retention of sodium observed during development is consequent primarily to enhanced tubular reabsorption rather than to low rates of glomerular filtration. The enhanced transport of sodium occurs in nephron segments located beyond the proximal tubule, apparently under the stimulation of the high plasma concentration of aldosterone. This adaptive mechanism may account for the fact that the infant thrives on a rather low intake of sodium, as prevails during the period of breast-feeding. The renin-angiotensin-aldosterone system cannot be fully inhibited even by intravascular volume expansion and this may account for the blunted natriuretic response of the developing animal and human to the acute infusion of saline or albumin solutions. Conversely, the renal sodium loss and the hyponatremia often encountered in premature babies appear to be due to an insufficient rise in aldosterone secretion or to a limited responsiveness of the distal tubule to aldosterone stimulation.
有证据表明，发育过程中观察到的钠潴留主要是由于肾小管重吸收增强，而非肾小球滤过率降低。钠转运增强发生在近端小管以外的肾单位节段，显然是在高血浆醛固酮浓度的刺激下。这种适应性机制可能解释了婴儿在钠摄入量相当低的情况下仍能茁壮成长的现象，母乳喂养期间就是如此。即使通过血管内容量扩张，肾素 - 血管紧张素 - 醛固酮系统也不能被完全抑制，这可能解释了发育中的动物和人类对急性输注生理盐水或白蛋白溶液的利钠反应减弱。相反，早产儿中经常遇到的肾钠丢失和低钠血症似乎是由于醛固酮分泌增加不足或远曲小管对醛固酮刺激的反应性有限。
