Direct determination of PCO2 in the rat renal cortex

T. D. DuBose, L. R. Pucacco, D. W. Seldin

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The mechanism by which the kidney reabsorbs sodium bicarbonate could be a result of: (a) H+ secretion, (b) direct HCO- 3 reabsorption, or (c) a combination of both processes. Most of the studies which have supported the H+ secretory theory have involved the assumption that tubular fluid and arterial PCO2 were equal. We have utilized a new PCO2 microelectrode to directly determine in situ PCO2 of tubular fluid and stellate vessel blood in the cortex of the rat kidney during control conditions and after alterations in acid-base status. In 21 control rats, proximal tubular fluid PCO2 exceeded systemic arterial PCO2 (ΔPCO2) by 25.9 ± 0.92 mm Hg (P < 0.001). The values obtained for both distal tubular fluid and stellate vessel blood were not significantly different from proximal tubular PCO2. Evaluation of PCO2 in the proximal tubules of Munich-Wistar rats did not reveal evidence for a declining profile for PCO2 along the length of the nephron. When proximal bicarbonate reabsorption was increased or decreased acutely by alterations in acid-base status, ΔPCO2 changed in parallel. Furthermore, benzolamide administration significantly reduced ΔPCO2. We conclude: (a) that the PCO2 in tubular fluid is significantly greater than systemic arterial PCO2 (b) that there is no tendency for the observed PCO2 to fall along the proximal tubule, (c) the mean PCO2 in the proximal and distal tubules as well as the stellate vessel is not significantly different, thereby rendering the concept of a 'diffusion barrier' for CO2 in the proximal tubule unlikely, and (d) the level of renal cortical PCO2 appears to vary directly with the magnitude of bicarbonate reabsorption.

Original languageEnglish (US)
Pages (from-to)338-348
Number of pages11
JournalJournal of Clinical Investigation
Volume62
Issue number2
StatePublished - 1978

Fingerprint

Bicarbonates
Blood Vessels
Benzolamide
Kidney
Kidney Cortex
Sodium Bicarbonate
Acids
Nephrons
Microelectrodes
Wistar Rats

ASJC Scopus subject areas

  • Medicine(all)

Cite this

DuBose, T. D., Pucacco, L. R., & Seldin, D. W. (1978). Direct determination of PCO2 in the rat renal cortex. Journal of Clinical Investigation, 62(2), 338-348.

Direct determination of PCO2 in the rat renal cortex. / DuBose, T. D.; Pucacco, L. R.; Seldin, D. W.

In: Journal of Clinical Investigation, Vol. 62, No. 2, 1978, p. 338-348.

Research output: Contribution to journalArticle

DuBose, TD, Pucacco, LR & Seldin, DW 1978, 'Direct determination of PCO2 in the rat renal cortex', Journal of Clinical Investigation, vol. 62, no. 2, pp. 338-348.
DuBose TD, Pucacco LR, Seldin DW. Direct determination of PCO2 in the rat renal cortex. Journal of Clinical Investigation. 1978;62(2):338-348.
DuBose, T. D. ; Pucacco, L. R. ; Seldin, D. W. / Direct determination of PCO2 in the rat renal cortex. In: Journal of Clinical Investigation. 1978 ; Vol. 62, No. 2. pp. 338-348.
@article{8f91898794ef406a88bf3b9aa49a22f0,
title = "Direct determination of PCO2 in the rat renal cortex",
abstract = "The mechanism by which the kidney reabsorbs sodium bicarbonate could be a result of: (a) H+ secretion, (b) direct HCO- 3 reabsorption, or (c) a combination of both processes. Most of the studies which have supported the H+ secretory theory have involved the assumption that tubular fluid and arterial PCO2 were equal. We have utilized a new PCO2 microelectrode to directly determine in situ PCO2 of tubular fluid and stellate vessel blood in the cortex of the rat kidney during control conditions and after alterations in acid-base status. In 21 control rats, proximal tubular fluid PCO2 exceeded systemic arterial PCO2 (ΔPCO2) by 25.9 ± 0.92 mm Hg (P < 0.001). The values obtained for both distal tubular fluid and stellate vessel blood were not significantly different from proximal tubular PCO2. Evaluation of PCO2 in the proximal tubules of Munich-Wistar rats did not reveal evidence for a declining profile for PCO2 along the length of the nephron. When proximal bicarbonate reabsorption was increased or decreased acutely by alterations in acid-base status, ΔPCO2 changed in parallel. Furthermore, benzolamide administration significantly reduced ΔPCO2. We conclude: (a) that the PCO2 in tubular fluid is significantly greater than systemic arterial PCO2 (b) that there is no tendency for the observed PCO2 to fall along the proximal tubule, (c) the mean PCO2 in the proximal and distal tubules as well as the stellate vessel is not significantly different, thereby rendering the concept of a 'diffusion barrier' for CO2 in the proximal tubule unlikely, and (d) the level of renal cortical PCO2 appears to vary directly with the magnitude of bicarbonate reabsorption.",
author = "DuBose, {T. D.} and Pucacco, {L. R.} and Seldin, {D. W.}",
year = "1978",
language = "English (US)",
volume = "62",
pages = "338--348",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "2",

}

TY - JOUR

T1 - Direct determination of PCO2 in the rat renal cortex

AU - DuBose, T. D.

AU - Pucacco, L. R.

AU - Seldin, D. W.

PY - 1978

Y1 - 1978

N2 - The mechanism by which the kidney reabsorbs sodium bicarbonate could be a result of: (a) H+ secretion, (b) direct HCO- 3 reabsorption, or (c) a combination of both processes. Most of the studies which have supported the H+ secretory theory have involved the assumption that tubular fluid and arterial PCO2 were equal. We have utilized a new PCO2 microelectrode to directly determine in situ PCO2 of tubular fluid and stellate vessel blood in the cortex of the rat kidney during control conditions and after alterations in acid-base status. In 21 control rats, proximal tubular fluid PCO2 exceeded systemic arterial PCO2 (ΔPCO2) by 25.9 ± 0.92 mm Hg (P < 0.001). The values obtained for both distal tubular fluid and stellate vessel blood were not significantly different from proximal tubular PCO2. Evaluation of PCO2 in the proximal tubules of Munich-Wistar rats did not reveal evidence for a declining profile for PCO2 along the length of the nephron. When proximal bicarbonate reabsorption was increased or decreased acutely by alterations in acid-base status, ΔPCO2 changed in parallel. Furthermore, benzolamide administration significantly reduced ΔPCO2. We conclude: (a) that the PCO2 in tubular fluid is significantly greater than systemic arterial PCO2 (b) that there is no tendency for the observed PCO2 to fall along the proximal tubule, (c) the mean PCO2 in the proximal and distal tubules as well as the stellate vessel is not significantly different, thereby rendering the concept of a 'diffusion barrier' for CO2 in the proximal tubule unlikely, and (d) the level of renal cortical PCO2 appears to vary directly with the magnitude of bicarbonate reabsorption.

AB - The mechanism by which the kidney reabsorbs sodium bicarbonate could be a result of: (a) H+ secretion, (b) direct HCO- 3 reabsorption, or (c) a combination of both processes. Most of the studies which have supported the H+ secretory theory have involved the assumption that tubular fluid and arterial PCO2 were equal. We have utilized a new PCO2 microelectrode to directly determine in situ PCO2 of tubular fluid and stellate vessel blood in the cortex of the rat kidney during control conditions and after alterations in acid-base status. In 21 control rats, proximal tubular fluid PCO2 exceeded systemic arterial PCO2 (ΔPCO2) by 25.9 ± 0.92 mm Hg (P < 0.001). The values obtained for both distal tubular fluid and stellate vessel blood were not significantly different from proximal tubular PCO2. Evaluation of PCO2 in the proximal tubules of Munich-Wistar rats did not reveal evidence for a declining profile for PCO2 along the length of the nephron. When proximal bicarbonate reabsorption was increased or decreased acutely by alterations in acid-base status, ΔPCO2 changed in parallel. Furthermore, benzolamide administration significantly reduced ΔPCO2. We conclude: (a) that the PCO2 in tubular fluid is significantly greater than systemic arterial PCO2 (b) that there is no tendency for the observed PCO2 to fall along the proximal tubule, (c) the mean PCO2 in the proximal and distal tubules as well as the stellate vessel is not significantly different, thereby rendering the concept of a 'diffusion barrier' for CO2 in the proximal tubule unlikely, and (d) the level of renal cortical PCO2 appears to vary directly with the magnitude of bicarbonate reabsorption.

UR - http://www.scopus.com/inward/record.url?scp=0018198971&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018198971&partnerID=8YFLogxK

M3 - Article

C2 - 670396

AN - SCOPUS:0018198971

VL - 62

SP - 338

EP - 348

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 2

ER -