Bengele H H, Schwartz J H, McNamara E R, Alexander E A
Am J Physiol. 1986 Jan;250(1 Pt 2):F115-9. doi: 10.1152/ajprenal.1986.250.1.F115.
We previously reported that acute respiratory acidosis (ARA) did not stimulate inner medullary collecting duct (IMCD) acidification. It was possible that the failure to find enhanced IMCD acidification was a function of insufficient buffer delivery. To answer this question we studied IMCD acidification in rats with ARA during the infusion of the buffer creatinine. We employed the microcatheterization technique to directly measure pH and PCO2 with glass membrane electrodes and also obtained fluid samples for the measurement of titratable acid and ammonium. Arterial pH was 7.19 +/- 0.01 and PCO2 was 93 +/- 2 mmHg. The IMCD data were analyzed as a function of IMCD length (approximately 6 mm). Equilibrium pH decreased from 5.99 +/- 0.05 to 5.58 +/- 0.02 and PCO2 increased from 71 +/- 11 to 132 +/- 6 mmHg between origin and tip. Bicarbonate delivery decreased from 111 +/- 14 to 38 +/- 2 nmol/min; titratable acid increased from 867 +/- 87 to 1,625 +/- 61 nmol/min, but ammonium delivery did not change along the duct. Thus, estimated net acid increased from 1,772 +/- 155 to 2,709 +/- 88 nmol/min. We conclude that during the presence of increased buffer delivery to the IMCD, rats with ARA markedly increased proton secretion along the terminal nephron.
