Questions and replies: renal mechanisms for urinary concentrating and diluting processes.
Mechanisms for urinary concentration or dilution depend on counterflow processes, both tubular and vascular, within the renal medulla. Recently, there have emerged differing hypotheses about the renal tubular processes responsible for maintaining a hypertonic medullary interstitium. In this Editorial Review, R.W. Berliner frames three questions germane to this issue, and J.P. Kokko and D.J. Marsh provide their responses to these queries. The major issues addressed are: 1) What are the major unresolved question(s) concerning the mechanism by which concentrated urine is formed? 2) Current evidence suggests that the urea concentration in thin ascending limbs is slightly lower in the lumen than in interstitial fluid. Is the transepithelial concentration gradient between thin ascending limb and renal medullary interstitium sufficient to permit an entirely passive mechanism for diluting tubular fluid in the thin ascending limb? 3) A simple three-compartment model for the renal medullary concentrating process would include the tubular lumen, peritubular capillary, and the interstitium. Is it possible to generate a model that, by juxtaposing medullary structures, might explain renal medullary counterflow processes more adequately than the simple three-compartment model?
D000818:Animals; D003377:Countercurrent Distribution; D006224:Cricetinae; D005110:Extracellular Space / Q000502:physiology; D007671:Kidney Concentrating Ability; D007679:Kidney Medulla / Q000098:blood supply / Q000502:physiology; D008138:Loop of Henle / Q000502:physiology; D008433:Mathematics; D051379:Mice; D008954:Models, Biological; D011817:Rabbits; D051381:Rats; D012039:Regional Blood Flow; D012965:Sodium Chloride / Q000502:physiology; D014508:Urea / Q000502:physiology
D012965:Sodium Chloride; D014508:Urea