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Articles in PresS, published online ahead of print August 6, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00162.2002
Submitted on April 29, 2002
Accepted on July 25, 2002
1 Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, NY, USA
* To whom correspondence should be addressed. E-mail: alan{at}nephron.med.cornell.edu.
A mathematical model of the rat CD has been developed by concatenating previously published models of cortical (Am. J. Physiol. 280:F1072, 2001), outer medullary (Am. J. Physiol. 279:F24, 2000), and inner medullary segments (Am. J. Physiol. 274:F841, 1998). Starting with end-distal tubular flow rate and composition, plus interstitial solute profiles, the model predicts urinary solute flows, including the buffer concentrations required to assess net acid excretion. In the model CD, the interstitial cortico-medullary osmotic gradient provides the basis for the flow effect on transport of several solutes. For substances which have an interstitial accumulation and which can have diffusive secretion (e.g. urea and NH+4), enhanced luminal flow increases excretion by decreasing luminal accumulation. For substances which are reabsorbed (e.g. K+ and HCO-3), and for which luminal accumulation can enhance reabsorption, increasing luminal flow again increases excretion by decreasing luminal solute concentration. In model calculations, flow-de-pendent increases in HCO-3 and NH+4 approximately balance, so that net acid excretion is little changed by flow, albeit at a higher urine pH. The model identifies delivery flow rate to the CD as a potent determinant of urine pH, with high flows blunting maximal acidification. At even modestly high flows (9 nl/min per tubule, with 6% of filtered Na+ entering the CD), the model cannot achieve a urine pH less than 5.5 unless the delivered HCO-3 concentration is extremely low (less than 2 mM). Nevertheless, simulation of Na2SO4 diuresis does yield both an increase in net acid excretion and a decrease in urine HCO-3 (i.e. a decrease in pH), despite the increase in urine flow. This model should provide a tool to examine hypotheses regarding transport defects underlying distal renal tubular acidosis.
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