Renal metabolism of citrate.
Our studies on renal handling of citrate have shown that: (1) citrate enters renal tubular cells from luminal fluid (reabsorption) and peritubular blood; (2) reabsorption becomes maximal, i.e., Tm-limited, at filtered loads 7 to 8 times the normal; (3) administration of malate stimulates net renal production of citrate, leading to release into urine (net secretion) and into peritubular blood; (4) acute metabolic alkalosis, induced while plasma citrate levels are above normal, depressess net citrate reabsorption, stimulates citrate release into peritubular blood and abolishes overall renal uptake of citrate; (5) essentially all citrate extracted by the kidney is converted to CO2 at endogenous circulating levels. This contribution is 15 per cent of the total renal CO2 production and is independent of chronic alterations in acid-base balance.
D000138:Acidosis / Q000378:metabolism; D000208:Acute Disease; D000471:Alkalosis / Q000378:metabolism; D000818:Animals; D002245:Carbon Dioxide / Q000096:biosynthesis / Q000097:blood; D002463:Cell Membrane Permeability; D002908:Chronic Disease; D002951:Citrates / Q000032:analysis / Q000097:blood / Q000378:metabolism*; D002952:Citric Acid Cycle; D004912:Erythrocytes / Q000032:analysis; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000098:blood supply / Q000378:metabolism*; D007672:Kidney Cortex / Q000032:analysis; D007684:Kidney Tubules / Q000166:cytology; D008293:Malates / Q000378:metabolism; D010101:Oxygen Consumption; D012039:Regional Blood Flow
D002951:Citrates; D008293:Malates; D002245:Carbon Dioxide