Tannen R L
Kidney Int. 1977 Jun;11(6):453-65. doi: 10.1038/ki.1977.63.
Renal ammonia production appears to be intimately related to potassium homeostasis, and the two may comprise the components of a closed loop regulatory system. Studies with both intact organisms and in vitro systems indicate that potassium depletion stimulates and chronic potassium-loading suppresses renal ammonia production. An increase in ammoniagenesis has been shown to decrease potassium excretion. These observations suggest that changes in potassium modulate ammonia production, which in turn maintains hydrogen ion homeostasis and influences potassium excretion. Potassium depletion increases rat renal cortical ammonia production by altering metabolism in fashion identical to metabolic acidosis, but there is no convincing evidence that both processes are mediated by similar changes in either cellular hydrogen ion or potassium concentration. By contrast, potassium-loading, which depresses ammonia production, appears to affect primarily the outer medulla, a region that is not influenced by potassium depletion. Thus, potassium-loading apparently affects different portions of the renal tubule than depletion does, but the specific mechanism and physiologic significance of the different sites of action is unknown.
肾脏氨的生成似乎与钾稳态密切相关，二者可能构成一个闭环调节系统的组成部分。对完整生物体和体外系统的研究表明，钾缺乏会刺激肾脏氨的生成，而长期钾负荷则会抑制肾脏氨的生成。氨生成增加已被证明会减少钾的排泄。这些观察结果表明，钾的变化调节氨的生成，进而维持氢离子稳态并影响钾的排泄。钾缺乏通过以与代谢性酸中毒相同的方式改变代谢来增加大鼠肾皮质氨的生成，但没有令人信服的证据表明这两个过程是由细胞内氢离子或钾浓度的类似变化介导的。相比之下，抑制氨生成的钾负荷似乎主要影响外髓质，而该区域不受钾缺乏的影响。因此，钾负荷显然比钾缺乏影响肾小管的不同部分，但不同作用部位的具体机制和生理意义尚不清楚。
