scholarly journals Hydrogen ion secretion by the collecting duct as a determinant of the urine to blood PCO2 gradient in alkaline urine.

1982 ◽  
Vol 69 (1) ◽  
pp. 145-156 ◽  
Author(s):  
T D DuBose
1981 ◽  
Vol 59 (3) ◽  
pp. 235-238 ◽  
Author(s):  
W. L. M. Robson ◽  
M. L. Halperin ◽  
B.J. Stinebaugh ◽  
M. B. Goldstein

The purpose of this study was to elucidate the mechanism whereby a potassium infusion led to an elevation in the urine minus blood (U – B) [Formula: see text] difference in alkaline urine of the rabbit. Rabbits given 9α-flurohydrocortisone 16 h prior to study had a significantly higher U – B [Formula: see text] than control rabbits. However, the U – B [Formula: see text] was increased further after potassium infusion. These results suggest that the increased collecting duet hydrogen ion secretion in the rabbit may in part have been induced by mineralocorticoids and in addition been influenced by increasing the potassium concentration.


1981 ◽  
Vol 20 (5) ◽  
pp. 636-642 ◽  
Author(s):  
Siu-Cheung Tam ◽  
Marc B. Goldstein ◽  
Bobby J. Stinebaugh ◽  
Ching-Bun Chen ◽  
André Gougoux ◽  
...  

1983 ◽  
Vol 61 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Andre Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
Marc Goldstein ◽  
Bobby Stinebaugh ◽  
...  

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary [Formula: see text]. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, [Formula: see text], and the urine minus blood [Formula: see text] difference (U-B [Formula: see text]) were lower during acute hypercapnia. In these experiments, the urine [Formula: see text] was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B [Formula: see text] was 5 ± 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary [Formula: see text] can modify this relationship.


1981 ◽  
Vol 20 (5) ◽  
pp. 643-648 ◽  
Author(s):  
André Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
Maria-Angelica Duran ◽  
Ching-Bun Chen ◽  
...  

1983 ◽  
Vol 245 (6) ◽  
pp. F670-F679 ◽  
Author(s):  
K. M. Madsen ◽  
C. C. Tisher

The collecting duct of the mammalian kidney is involved in urine acidification. Recent studies in the turtle bladder suggest that hydrogen ion secretion in response to elevated CO2 is regulated by insertion of hydrogen pumps into the luminal membrane of the mitochondria-rich cells. Because intercalated cells of the collecting duct are structurally similar to mitochondria-rich cells of the amphibian bladder, we studied the rat outer medullary collecting duct (OMCD) during respiratory acidosis to determine whether changes compatible with hydrogen ion secretion occur in the intercalated cells. Rats were studied during normal acid-base conditions and after 4-5 h of respiratory acidosis. After collection of physiologic data, the kidneys were fixed by in vivo perfusion and processed for electron microscopy. No changes were observed in the principal cells of the OMCD. Morphometric analysis revealed a significant increase in the surface density of the apical plasma membrane and a decrease in the number of tubulovesicular profiles in the apical region of the intercalated cells throughout the OMCD with respiratory acidosis. There were no changes in surface density of the basolateral membrane. These findings suggest that in response to respiratory acidosis there is transport of membrane from the tubulovesicular membrane compartment to the apical plasma membrane of the intercalated cells.


1977 ◽  
Vol 52 (2) ◽  
pp. 119-123
Author(s):  
B. J. Stinebaugh ◽  
T. H. Hostetter ◽  
R. A. Peraino ◽  
F. X. Schloeder ◽  
W. N. Suki

1. The Pco2 gradient between alkaline urine and arterial blood (U—B Pco2) is thought to depend primarily on distal hydrogen ion secretion. However, other variables affecting the U—B Pco2 include the urine flow rate, the urinary bicarbonate and phosphate excretion rates and the glomerular filtration rate. 2. In order to evaluate the effects of acute changes in these factors on the U—B Pco2, bicarbonate-loaded dogs with maximal U—B Pco2 values were subjected to either acute unilateral elevations of ureteral pressure or hypotension caused by nitroprusside infusion. The results demonstrate that acute reduction in the glomerular fiitration rate does not cause a decrease in the U—B Pco2 as long as the urinary concentrations of phosphate and bicarbonate do not decline. 3. Urinary concentrations of phosphate and bicarbonate appeared more important than their excretion rates in the maintenance of elevated U—B Pco2 values.


1995 ◽  
Vol 6 (2) ◽  
pp. 295-301
Author(s):  
P E DeFranco ◽  
L Haragsim ◽  
P G Schmitz ◽  
B Bastani

Distal renal tubular acidosis (dRTA) is a common complication of autoimmune connective tissue diseases. The underlying pathophysiology of renal tubular acidosis in these syndromes is frequently characterized by impaired hydrogen ion secretion, i.e., secretory defect dRTA. However, the precise molecular events leading to this disturbance remain poorly understood. An opportunity was recently afforded to examine the ultrastructural features of the collecting duct in a patient with Sjögren's syndrome and secretory defect dRTA. Immunocytochemical analysis of a renal biopsy obtained 12 months after the patient's initial presentation demonstrated a complete absence of vacuolar H(+)-ATPase in the collecting duct. Antibodies to the 31- and 56-kd kidney-specific subunits of the H(+)-ATPase pump were used to characterize pump distribution. Interestingly, although antiserum to the CI-:HCO3- anion exchanger (band-3 protein) reacted strongly with normal human kidney and the patient's red blood cells, no immunoreactivity was observed in the patient's collecting duct epithelium. Importantly, electron microscopy of the patient's renal biopsy specimen disclosed cells that ultrastructurally were indistinguishable from intercalated cells. These results suggest that the functional basis of impaired hydrogen ion secretion in this patient was secondary to the absence of intact H(+)-ATPase pumps rather than defective pump function or distribution. The presence of intercalated cells ultrastructurally, but the absence of discernible staining for band-3 protein and H(+)-ATPase, also suggests that the defect in proton secretion may represent a defect involving the assembly of at least two of the ion transport pumps essential for the normal maintenance of acid-base homeostasis by the intercalated cells.(ABSTRACT TRUNCATED AT 250 WORDS)


1978 ◽  
Vol 235 (3) ◽  
pp. F203-F208
Author(s):  
J. T. Sehy ◽  
M. K. Roseman ◽  
J. A. Arruda ◽  
N. A. Kurtzman

The effect of acute respiratory alkalosis (ARA) on distal nephron H+ secretion was evaluated by measuring urine-to-blood (U-B) Pco2 in dogs with highly alkaline urine (urine pH greater than 7.8). ARA led to a significant decrease in U-B Pco2 and in urine HCO3 concentration; urine pH, however, increased significantly, indicating that the decrease in urine Pco2 was of greater magnitude than the decrease in urine HCO3 concentration. For any given urine HCO3 concentration urine Pco2 was lower (i.e., urine pH was higher) in ARA than in controls. Administration of tris(hydroxymethyl)aminomethane (Tris) during ARA resulted in a significant increase in U-B Pco2 to control values. In animals with moderately alkaline urine (urine pH 6.4--7.4) and high urine PO4 concentration, ARA resulted in a significant decrease in UB-Pco2 and urine PO4 concentrations. Neutral PO4 infusion in these dogs resulted in an increase in urine PO4 concentration and U-B Pco2 to control levels. These data demonstrate that ARA results in a significant decrease in U-B Pco2 that is not solely attributable to changes in urine HCO3 concentration. The observation that Tris and PO4 infusion during ARA raises U-B Pco2 to control levels suggests that the ability to secrete H+ is intact.


1981 ◽  
Vol 241 (6) ◽  
pp. F659-F668 ◽  
Author(s):  
M. L. Graber ◽  
H. H. Bengele ◽  
J. H. Schwartz ◽  
E. A. Alexander

To directly characterize acidification by the collecting duct, we developed pH and PCO2 microelectrodes suitable for microcatheterization of the inner medullary collecting duct (IMCD). In saline-infused control rats apparent in situ pH fell significantly along the IMCD, from 5.95 at 60% length to 5.49 at the papilla tip. Luminal PCO2 averaged 34 +/- 1 mmHg and PD averaged +3 mV. In rats acutely infused with 0.1 N HCl, apparent in situ pH also decreased significantly from 5.56 to 5.28, PD averaged +2 mV, and luminal PCO2 31 +/- 1 mmHg. The luminal PCO2 of HCl-infused rats was significantly less than controls and both levels were significantly below arterial PCO2. Corroborating the in situ pH profiles, equilibrium pH measured on collected IMCD samples also decreased significantly with percent length. In samples measured in situ and at equilibrium, a small but significant acid disequilibrium pH ws seen in both groups. We interpret these results to indicate that the IMCD actively participates in distal acidification. It is proposed that acidification by the IMCD is predominantly mediated by hydrogen ion secretion which simultaneously acidifies luminal fluid and generates a cellular sink for CO2, thereby inducing an acid disequilibrium pH by two mechanisms.


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