Will P C, Cortright R N, Groseclose R G, Hopfer U
Am J Physiol. 1985 Jan;248(1 Pt 1):G133-41. doi: 10.1152/ajpgi.1985.248.1.G133.
Secondary hyperaldosteronism produced by Na+ depletion was associated with increases in salt and fluid absorption in both the small intestine and the distal colon but not in the cecum and the proximal colon. Because these changes had not been documented for the small intestine, this study focused on the regulation of this tissue. Increased NaCl and water absorption was expressed in vitro by increases in short-circuit current and transepithelial potential and in vivo by increased fluid absorption and a decreased luminal content of Na+ and water. For example, the short-circuit current in the ileum of Na+-depleted rats was 2-fold that of adrenalectomized and 1.3-fold that of adrenal-intact control animals. The short-circuit current was inhibitable 24 +/- 14% by micromolar concentrations of amiloride in Na+-deficient animals compared with 1 +/- 3% in control animals. Similarly, ileal fluid absorption in vivo was 2.3-fold higher in Na+-deficient relative to control animals. The additional fluid absorption was sensitive to 50 microM amiloride, whereas amiloride had no effect in control animals. Furthermore, the Na+ content of the chyme from the ileum of Na+-deficient animals was about half that of controls. These results suggest that mineralocorticoids can induce the amiloride-sensitive Na+ transporter in the small intestine and that this type of epithelial salt transport can become a major pathway for salt retention by the small intestine.
由钠缺乏引起的继发性醛固酮增多症与小肠和远端结肠中盐和液体吸收增加有关，但盲肠和近端结肠未出现这种情况。由于小肠的这些变化此前未被记录，本研究聚焦于该组织的调节。体外，氯化钠和水吸收增加表现为短路电流和跨上皮电位升高；体内则表现为液体吸收增加以及肠腔内钠和水含量降低。例如，钠缺乏大鼠回肠的短路电流是肾上腺切除大鼠的2倍，是肾上腺完整对照动物的1.3倍。与对照动物的1±3%相比，微摩尔浓度的氨氯吡咪可使钠缺乏动物的短路电流抑制24±14%。同样，钠缺乏动物回肠的体内液体吸收相对于对照动物高2.3倍。额外的液体吸收对50微摩尔氨氯吡咪敏感，而氨氯吡咪对对照动物无影响。此外，钠缺乏动物回肠食糜中的钠含量约为对照动物的一半。这些结果表明，盐皮质激素可诱导小肠中氨氯吡咪敏感的钠转运体，且这种上皮性盐转运可成为小肠保留盐分的主要途径。
