Sonnenberg H, Honrath U, Wilson D R
Kidney Int. 1987 May;31(5):1121-5. doi: 10.1038/ki.1987.117.
The in vivo microcatheterization technique was used to study amiloride-induced transport alterations in the inner medullary collecting duct. Amiloride treated rats (0.1 mg/hr) had significant diuresis and natriuresis, as well as antikaliuresis, compared to untreated controls. The relative decrease in potassium excretion was associated with a significant rise in plasma potassium concentration. Net sodium transport in the duct was decreased from 83 + 3 to 46 + 6 per cent of delivered load, as a result of amiloride treatment. Smaller, but statistically significant, reductions (P less than 0.01) were seen for fluid and chloride reabsorptions (from 66 + 3 to 51 + 4%, and from 72 + 4 to 52 + 5%, respectively). Potassium reabsorption increased from 15 + 8 to 61 + 6% of delivered load. The data indicated that amiloride natriuresis is determined primarily by inhibition of sodium reabsorption in the medullary collecting duct, probably due to blockade of a specific Na channel. The antikaliuresis, on the other hand, appears to be due to inhibition of secretion both in upstream nephron segments and in the duct itself.
采用体内微导管插入技术研究氨氯吡咪对髓质集合管转运的影响。与未治疗的对照组相比，接受氨氯吡咪治疗的大鼠（0.1毫克/小时）出现显著的利尿、利钠以及抗尿钾作用。钾排泄的相对减少与血浆钾浓度的显著升高相关。由于氨氯吡咪治疗，集合管中的钠净转运从输送负荷的83% + 3%降至46% + 6%。液体和氯的重吸收也有较小但具有统计学意义的降低（P小于0.01）（分别从66% + 3%降至51% + 4%，以及从72% + 4%降至52% + 5%）。钾重吸收从输送负荷的15% + 8%增加至61% + 6%。数据表明，氨氯吡咪利尿主要是通过抑制髓质集合管中的钠重吸收来实现的，这可能是由于阻断了特定的钠通道。另一方面，抗尿钾作用似乎是由于抑制了上游肾单位节段和集合管本身的分泌。
