Vinay P, Lemieux G, Gougoux A, Halperin M
Kidney Int. 1986 Jan;29(1):68-79. doi: 10.1038/ki.1986.9.
In summary, we propose: that renal ammoniagenesis is regulated both by factors dependent and independent of the acid-base status, the net effect of the ammoniagenic process on the proton balance being directly related to the rate of urinary ammonium excretion; that the renal metabolism of glutamine should not be examined independently of the metabolism of other substrate physiologically taken up by the kidney; that different pathways for glutamine metabolism will change during acid-base disorders of organic or nonorganic origin; that, among the main glutamine utilizing pathways, only the GLDH pathway is influenced directly by the acid-base status; the ammoniagenic transamination pathways is regulated by substrate availability in the kidney; that the lowest ammoniagenic flux in the kidney coincides with the rate of alanine production since alanine appears to derive directly from glutamine. When this pathway is stimulated without concomitant acidosis, most of the ammonia produced is not excreted in urine but released in the renal venous blood: thus, no significant effect on the acid-base balance is produced; that glutamine is metabolized by proximal kidney tubules of acidotic dogs probably through net oxidation; that the quantitative analysis of the metabolic consequence of this process indicates that the rate of ATP turnover at this site may effectively place an upper limit to the rate of glutamine oxidation, and ammonia production by the kidney, and that this limit is nearly reached in chronically acidotic animals.
总之，我们提出：肾氨生成受依赖和不依赖酸碱状态的因素调节，氨生成过程对质子平衡的净效应与尿铵排泄率直接相关；不应脱离肾脏生理摄取的其他底物的代谢来单独研究谷氨酰胺的肾代谢；在有机或非有机源性酸碱紊乱期间，谷氨酰胺代谢的不同途径会发生变化；在主要的谷氨酰胺利用途径中，只有谷氨酸脱氢酶（GLDH）途径直接受酸碱状态影响；氨生成转氨途径受肾脏中底物可用性的调节；肾脏中最低的氨生成通量与丙氨酸生成速率一致，因为丙氨酸似乎直接来源于谷氨酰胺。当该途径在无伴随酸中毒的情况下受到刺激时，产生的大部分氨不是通过尿液排泄，而是释放到肾静脉血中：因此，对酸碱平衡没有显著影响；酸中毒犬的近端肾小管可能通过净氧化作用代谢谷氨酰胺；对该过程代谢后果的定量分析表明，该部位的ATP周转速率可能有效地对谷氨酰胺氧化速率和肾脏氨生成速率设置上限，并且在慢性酸中毒动物中几乎达到了这个极限。
