Studies on the regulation of hydrogen ion secretion in the collecting duct in vivo: Evaluation of factors that influence the urine minus blood PCO2 difference

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.

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Cellular response to acute respiratory acidosis in rat medullary collecting duct

AJP Renal Physiology ◽

10.1152/ajprenal.1983.245.6.f670 ◽

1983 ◽

Vol 245 (6) ◽

pp. F670-F679 ◽

Cited By ~ 8

Author(s):

K. M. Madsen ◽

C. C. Tisher

Keyword(s):

Plasma Membrane ◽

Surface Density ◽

Collecting Duct ◽

Respiratory Acidosis ◽

Hydrogen Ion ◽

Apical Plasma Membrane ◽

Apical Region ◽

Intercalated Cells ◽

Ion Secretion ◽

Medullary Collecting Duct

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.

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

Journal of Clinical Investigation ◽

10.1172/jci110425 ◽

1982 ◽

Vol 69 (1) ◽

pp. 145-156 ◽

Cited By ~ 60

Author(s):

T D DuBose

Keyword(s):

Collecting Duct ◽

Hydrogen Ion ◽

Alkaline Urine ◽

Ion Secretion

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Absence of vacuolar H(+)-ATPase pump in the collecting duct of a patient with hypokalemic distal renal tubular acidosis and Sjögren's syndrome.

Journal of the American Society of Nephrology ◽

10.1681/asn.v62295 ◽

1995 ◽

Vol 6 (2) ◽

pp. 295-301

Author(s):

P E DeFranco ◽

L Haragsim ◽

P G Schmitz ◽

B Bastani

Keyword(s):

Renal Biopsy ◽

Renal Tubular Acidosis ◽

Collecting Duct ◽

Band 3 ◽

Distal Renal Tubular Acidosis ◽

Hydrogen Ion ◽

Intercalated Cells ◽

Band 3 Protein ◽

Ion Secretion ◽

Renal Tubular

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)

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Relationship of urinary and blood carbon dioxide tension during hypercapnia in the rat. Its significance in the evaluation of collecting duct hydrogen ion secretion.

Journal of Clinical Investigation ◽

10.1172/jci111856 ◽

1985 ◽

Vol 75 (5) ◽

pp. 1517-1530 ◽

Cited By ~ 12

Author(s):

D C Batlle ◽

M Downer ◽

C Gutterman ◽

N A Kurtzman

Keyword(s):

Carbon Dioxide ◽

Collecting Duct ◽

Carbon Dioxide Tension ◽

Hydrogen Ion ◽

Ion Secretion ◽

Relationship Of

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pH and PCO2 profiles of the rat inner medullary collecting duct

AJP Renal Physiology ◽

10.1152/ajprenal.1981.241.6.f659 ◽

1981 ◽

Vol 241 (6) ◽

pp. F659-F668 ◽

Cited By ~ 1

Author(s):

M. L. Graber ◽

H. H. Bengele ◽

J. H. Schwartz ◽

E. A. Alexander

Keyword(s):

Collecting Duct ◽

Hydrogen Ion ◽

Arterial Pco2 ◽

Inner Medullary Collecting Duct ◽

Ion Secretion ◽

Medullary Collecting Duct ◽

Disequilibrium Ph ◽

Ph Profiles

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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Effect of mineralocorticoids on collecting duct hydrogen ion secretion in the rabbit

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y81-037 ◽

1981 ◽

Vol 59 (3) ◽

pp. 235-238 ◽

Cited By ~ 1

Author(s):

W. L. M. Robson ◽

M. L. Halperin ◽

B.J. Stinebaugh ◽

M. B. Goldstein

Keyword(s):

Potassium Concentration ◽

Collecting Duct ◽

Hydrogen Ion ◽

Alkaline Urine ◽

Ion Secretion

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.

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Phosphate transport along the inner medullary collecting duct of the rat

AJP Renal Physiology ◽

10.1152/ajprenal.1979.237.1.f48 ◽

1979 ◽

Vol 237 (1) ◽

pp. F48-F54

Author(s):

H. H. Bengele ◽

C. P. Lechene ◽

E. A. Alexander

Keyword(s):

Renal Mass ◽

Collecting Duct ◽

Phosphate Transport ◽

In Vivo Evaluation ◽

Phosphate Absorption ◽

Inner Medullary Collecting Duct ◽

Nephron Segment ◽

Medullary Collecting Duct ◽

Significant Change

The question of phosphate transport along the collecting duct remains controversial inasmuch as no data from direct in vivo evaluation of this nephron segment have been reported. We measured net phosphate transport along the inner medullary collecting duct (IMCD) using the collecting duct microcatheterization technique in five groups of rats. In control rats no net phosphate transport was found and 9.4% of the fraction of filtered phosphate (FFP) entered the IMCD and was excreted. After acute thyroparathyroidectomy (TPTX) there was a striking reduction in the FFP entering the IMCD, 1.8%, and significant reabsorption occurred, 0.5% being excreted. With acute TPTX and parathormone infusion, delivery increased to 33% without significant change along the IMCD. With acute TPTX and phosphate infusion, delivery was increased to control levels but no change was found in net phosphate transport. In rats studied 5-7 days after uninephrectomy alone, phosphate delivery was greater than in control, 25%, and no net phosphate transport was found. These studies demonstrate that phosphate absorption occurs along the IMCD in acutely TPTX rats when the delivery of phosphate to the IMCD is markedly reduced. The increase in phosphaturia which occurs after a reduction in renal mass cannot be accounted for by changes in net phosphate transport along the IMCD.

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