Peritubular pH and PCO'2 in renal tubular acidification.
The influence of peritubular capillary pH and PCO'2 on renal tubular acidification was studied in rats by luminal and peritubular perfusion techniques.  Luminal stopped-flow microperfusions were carried out with bicarbonate or alkaline phosphate solutions and luminal pH continuously measured by antimony micorelectrodes.  Peritubular calpillary microperfusions were carried out with mammalian Ringer solution kept at different pH and PCO'2.  The acidification process was assessed in terms of 1)maximal pH differences, 2)rates of pH change, and 3)rates of bicarbinate reabsorption or H'+ ion secretion.  During peritubular perfusions at physiological pH and PCO'2 tubular  acidifying capacity was maintained at near-normal levels.  Perfusingcapillaries at high pH and low PCO'2, especially with bicarbonate Ringer, acidification was markedly depressed; it was moderately reduced at a peritubular pH of 5.6.  At a capillary pH of 7.4, acidification was similiar at low and physiological PCO'2and enhanced at elevated PCO'2.  Systemic respiratory acidosis enhanced acidification in the proximal tubule, but reduced it in distal segments.
D000136:Acid-Base Equilibrium; D000142:Acidosis, Respiratory / Q000503:physiopathology; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D002245:Carbon Dioxide / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007684:Kidney Tubules / Q000502:physiology*; D007686:Kidney Tubules, Distal / Q000503:physiopathology; D007687:Kidney Tubules, Proximal / Q000503:physiopathology; D008297:Male; D008839:Microelectrodes; D010313:Partial Pressure; D010477:Perfusion; D010710:Phosphates / Q000494:pharmacology; D051381:Rats
D001639:Bicarbonates; D010710:Phosphates; D002245:Carbon Dioxide