Effects of saline infusion on titratable acid generation and ammonia secretion.
Short-term hyperchloremic metabolic acidosis can decrease sodium reabsorption by the superficial proximal tubule (PT), increase tubular fluid flow rate, and stimulate aldosterone release. We studied the effects of increased tubular fluid delivery (graded saline infusion) and mineralocorticosteroid administration on tubular fluid pH (TFpH), titratable acid (TA) generation, and ammonium (NH+4) secretion by superficial proximal and distal tubules (DT) of acidotic, phosphate-loaded rats. The TFpH was 6.4 +/- 0.1 at the late proximal tubule (LP); it was unaltered at the early (ED) or late distal tubule (LD), but urine pH (UpH) was 1 unit lower. The major fraction of TA or NH+4 was formed in the superficial PT. There was no net TA generation by the superficial DT even during supplemental mineralocorticosteroid and increased Pi delivery during saline infusion. TA excretion was increased only slightly by saline infusion in acidotic rats despite increased buffer delivery (caused by decreased Pi reabsorption, primarily in the loop segment) because this was offset by a rise in UpH. Ammonia was secreted into tubular fluid in the superficial PT and DT; there was loss of NH+4 in the loop segment and addition after the LD. Saline infusion did not modify TFpH in the PT or DT but increased NH+4 secretion by the DT in direct proportion to tubular fluid flow. DOCA administration increased the addition of NH+4 between the LD and the urine. In conclusion 1) the superficial PT is of major importance for acidification, generation of TA, and secretion of NH+4 in short-term metabolic acidosis. 2) The superficial DT does not generate TA even during dramatically high rates of buffer delivery and mineralocorticosteroid administration. 3) Excretion of NH+4 is increased by saline infusion, which leads to flow-dependent NH+4 secretion by the superficial DT. 4) Chronic administration of DOCA stimulates NH+4 secretion predominantly in the terminal or deep nephrons.
D000141:Acidosis, Renal Tubular / Q000378:metabolism; D000143:Acids / Q000378:metabolism* / Q000652:urine; D000450:Aldosterone / Q000494:pharmacology; D000641:Ammonia / Q000378:metabolism*; D000818:Animals; D001826:Body Fluids / Q000378:metabolism; D002021:Buffers; D003900:Desoxycorticosterone / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007668:Kidney / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism*; D007686:Kidney Tubules, Distal / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D011188:Potassium / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology*
D000143:Acids; D002021:Buffers; D010710:Phosphates; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D000450:Aldosterone; D000641:Ammonia; D011188:Potassium