Effects of Chloride Restriction and Depletion on Acid-Base Balance and Chloride Conservation in the Rat

1970 ◽  
Vol 38 (3) ◽  
pp. 385-396 ◽  
Author(s):  
R. G. Luke ◽  
Y. Warren ◽  
M. Kashgarian ◽  
H. Levitin
Keyword(s):  
Proximal Tubule ◽  
Respiratory Acidosis ◽  
Dietary Sodium ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Plasma Bicarbonate ◽  
Chloride Depletion ◽  
Plasma Chloride ◽  
Urinary Acid ◽  
Net Acid Excretion

1. In the rat dietary chloride restriction has been shown to cause an elevation of the plasma bicarbonate and urinary net acid excretion, provided dietary sodium is available. Likewise the degree of elevation of plasma bicarbonate during chloride depletion, produced by prior exposure to 8% CO2 for 24 hr, was dependent on whether sodium (as the neutral phosphate) was or was not being ingested. 2. Correction of the hypochloraemia and the elevated plasma bicarbonate following exposure to CO2 and subsequent recovery on a low chloride diet is more complete in the rat than the dog. Evidence is presented that the plasma chloride rises in the rat because of the movement of chloride out of intracellular sites, and that chloride depletion and/or the associated metabolic alkalosis elevates endogenous acid production. 3. Chloride depleted rats were re-exposed to 8% CO2 in air. Renal chloride conservation remained intact. The hypochloraemia and rise in plasma bicarbonate in response to CO2 were not dependent on chloruresis although urinary acid excretion and the rise in serum bicarbonate were inhibited when the plasma chloride did not fall. 4. Consideration of these experiments with the related micropuncture experiments of Warren et al. (1970) suggests that: (a) the intimate relationship between hypochloraemia and the elevation of plasma bicarbonate in respiratory acidosis is related to reciprocal changes in proximal tubular absorption of chloride and bicarbonate; (b) chloride depletion can increase bicarbonate absorption in the proximal tubule and urinary net acid excretion; (c) a rise in TF/P Cl in the proximal tubule does not necessarily correlate with changes in external chloride balance; (d) the distal chloride conserving mechanism is unaffected by rates of sodium or phosphate excretion, exposure to carbon dioxide, or increases in the rate of tubular bicarbonate absorption.

Micropuncture Studies of Chloride and Bicarbonate Absorption in the Proximal Renal Tubule of the Rat in Respiratory Acidosis and in Chloride Depletion

1970 ◽  
Vol 38 (3) ◽  
pp. 375-383 ◽  
Author(s):  
Y. Warren ◽  
R. G. Luke ◽  
M. Kashgarian ◽  
H. Levitin
Keyword(s):  
Proximal Tubule ◽  
Respiratory Acidosis ◽  
Maximum Plasma ◽  
Plasma Bicarbonate ◽  
Chloride Depletion ◽  
Chloride Absorption ◽  
Chloride Excretion ◽  
Proximal Tubular ◽  
Plasma Chloride ◽  
Urinary Acid

1. Micropuncture studies of chloride and bicarbonate absorption in the proximal tubule under free flow conditions were performed during exposure to 12% CO2 in air, during recovery from CO2 on a low chloride diet with and without concomitant sodium restriction, and during re-exposure to 12% CO2 in air with continuing chloride restriction. 2. After 3 hr of exposure to CO2 there was a significant increase in the TF/P Cl (ratio of tubular fluid to plasma chloride) in the proximal tubule and a significant increase in urinary chloride excretion with a drop in the plasma chloride. Maximum plasma bicarbonate and TF/P Cl levels were reached at 24 hr with no further increase after 48 hr exposure to CO2. Bicarbonate absorption in the proximal tubule formed a reciprocal pattern to chloride absorption. 3. It is concluded, in conjunction with the accompanying balance experiments of Luke et al. (1970), that a rising TF/P Cl in the proximal tubule correlates with increasing proximal tubular absorption of bicarbonate, a rising plasma bicarbonate, and an increasing urinary acid excretion, but not necessarily with external chloride balance, which is regulated by a more distal site in the nephron. In respiratory acidosis and chloride depletion the TF/P Cl in the proximal tubule reflects the intratubular dynamics which influence bicarbonate absorption.

Role of citrate excretion in acid-base balance in diuretic-induced alkalosis in the rat

1985 ◽  
Vol 248 (6) ◽  
pp. F796-F803 ◽  
Author(s):  
A. M. Kaufman ◽  
C. Brod-Miller ◽  
T. Kahn
Keyword(s):  
Base Line ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Base Balance ◽  
Furosemide Administration ◽  
Net Acid Excretion

Studies were performed to assess the role of changes in the excretion of citrate, a metabolic precursor of bicarbonate, in acid-base balance in diuretic-induced metabolic alkalosis. Rats on a low-chloride diet with sodium sulfate added were studied during a base-line period, 3 days of furosemide administration, and 4 days post-furosemide. During the period of furosemide administration, net acid excretion and plasma bicarbonate concentration increased. In the post-furosemide period, net acid excretion remained higher than base line but plasma bicarbonate concentration did not increase further. Citrate excretion was significantly higher in the post-furosemide period than in base line. Studies substituting sodium neutral phosphate or sodium bicarbonate for dietary sodium sulfate demonstrated greater increases in net acid excretion post-furosemide and, again, no increase in plasma bicarbonate concentration during this period. Citrate excretion was greater than in the sulfate group. The increment in citrate excretion was proportional to the base “load,” defined with respect to changes in net acid excretion and/or dietary bicarbonate. Thus, in these studies alterations of base excretion in the form of citrate play an important role in acid-base balance during diuretic-induced metabolic alkalosis.

scholarly journals Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule

2007 ◽  
Vol 292 (4) ◽  
pp. F1256-F1266 ◽  
Author(s):  
Sophie de Seigneux ◽  
Hans Malte ◽  
Henrik Dimke ◽  
Jørgen Frøkiær ◽  
Søren Nielsen ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Collecting Duct ◽  
Chloride Concentration ◽  
Respiratory Acidosis ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Collecting Ducts ◽  
Chloride Excretion ◽  
Plasma Chloride

The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO2 and 13% O2 (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 ± 0.01 vs. 7.39 ± 0.01, P = 0.03), blood HCO3− concentration was increased (42 ± 0.9 vs. 32 ± 0.24 mM, P < 0.001), arterial Pco2 was increased (10.76 ± 0.4 vs. 7.20 ± 0.4 kPa, P < 0.001), and plasma chloride concentration was decreased (92.2 ± 0.7 vs. 97.2 ± 0.5 mM, P < 0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 ± 22 vs. 100 ± 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 ± 10 vs. 100 ± 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 ± 9 vs. 100 ± 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis.

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus)

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman
Keyword(s):  
Plasma Osmolality ◽  
Respiratory Acidosis ◽  
Electrolyte Balance ◽  
Plasma Composition ◽  
Total Plasma ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Base Balance

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.

Role of organic anions in renal response to dietary acid and base loads

1989 ◽  
Vol 257 (2) ◽  
pp. F170-F176 ◽  
Author(s):  
J. C. Brown ◽  
R. K. Packer ◽  
M. A. Knepper
Keyword(s):  
Organic Anion ◽  
Organic Anions ◽  
Acid Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urine Ph ◽  
Renal Response ◽  
Base Balance ◽  
Net Acid Excretion

Bicarbonate is formed when organic anions are oxidized systemically. Therefore, changes in organic anion excretion can affect systemic acid-base balance. To assess the role of organic anions in urinary acid-base excretion, we measured urinary excretion in control rats, NaHCO3-loaded rats, and NH4Cl-loaded rats. Total organic anions were measured by the titration method of Van Slyke. As expected, NaHCO3 loading increased urine pH and decreased net acid excretion (NH4+ + titratable acid - HCO3-), whereas NH4Cl loading had the opposite effect. Organic anion excretion was increased in response to NaHCO3 loading and decreased in response to NH4Cl loading. We quantified the overall effect of organic ion plus inorganic buffer ion excretion on acid-base balance. The amounts of organic anions excreted by all animals in this study were greater than the amounts of NH4+, HCO3-, or titratable acidity excreted. In addition, in response to acid and alkali loading, changes in urinary organic anion excretion were 40-50% as large as changes in net acid excretion. We conclude that, in rats, regulation of organic anion excretion can contribute importantly to the overall renal response to acid-base disturbances.

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.

Effect of acute thyroparathyroidectomy on nephron acidification

1984 ◽  
Vol 246 (5) ◽  
pp. F569-F574 ◽  
Author(s):  
H. H. Bengele ◽  
E. R. McNamara ◽  
E. A. Alexander
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Acid Excretion ◽  
Acid Phosphate ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Net Acid Excretion

The effect of the absence of parathyroid hormone on nephron acidification was determined in rats after acute thyroparathyroidectomy (TPTX). Tubular fluid samples were obtained from the superficial late proximal tubule (LPT), the early distal tubule ( EDT ), and along the inner medullary collecting duct (IMCD), and the results were compared with those obtained from control rats. In the LPT after TPTX, pH was lower, 6.66 +/- 0.01 vs. 6.73 +/- 0.01, and ammonium and net acid delivery were increased significantly. In the EDT no differences in pH, bicarbonate, or net acid were found between groups, whereas ammonium and acid phosphate were significantly different. Along the IMCD in control rats, pH decreased from 6.58 to 5.21 and the addition of about 430 nmol/min of net acid was observed. After TPTX more net acid entered the duct and pH was lower, 5.66, but did not change; neither did the amount of bicarbonate, ammonium, acid phosphate, or net acid change significantly along the duct. Net acid excretion was not different, however, among groups. These results demonstrate that TPTX markedly affects nephron acidification, increasing net acid along the proximal tubule. In contrast to that in control rats, however, net acidification is completed prior to the IMCD. We conclude that the acute absence of parathyroid hormone may significantly affect local nephron acidification but does not alter acid excretion.

Intercalated cell H+/OH− transporter expression is reduced in Slc26a4 null mice

2005 ◽  
Vol 289 (6) ◽  
pp. F1262-F1272 ◽  
Author(s):  
Young-Hee Kim ◽  
Jill W. Verlander ◽  
Sharon W. Matthews ◽  
Ira Kurtz ◽  
Wonkyong Shin ◽  
...  
Keyword(s):  
Protein Expression ◽  
Apical Region ◽  
Intercalated Cells ◽  
Acid Excretion ◽  
Type B ◽  
Wild Type ◽  
Acid Base Balance ◽  
Intercalated Cell ◽  
Transporter Expression ◽  
Net Acid Excretion

Slc26a4 ( Pds) encodes pendrin, a Cl−/HCO3− exchanger expressed in the apical region of type B and non-A, non-B cells, which mediates secretion of OH− equivalents. Thus genetic disruption of Slc26a4 leads to systemic alkalosis in some treatment models. However, humans and mice with genetic disruption of Slc26a4 have normal acid-base balance under basal conditions. Thus we asked: 1) Is net acid excretion altered in Slc26a4 (−/−) mice under basal conditions? 2) In the absence of pendrin-mediated OH− secretion, are increases in intracellular and systemic pH minimized through changes in intercalated cell subtype abundance or intercalated cell H+/OH− transporter expression? To answer these questions, net acid excretion and H+/OH− transporter expression were examined in Slc26a4 (−/−) and Slc26a4 (+/+) mice using balance studies, immunolocalization, and immunoblotting. Excretion of ammonium, titratable acid, and citrate were the same in Slc26a4 null and wild-type mice. However, urinary pH and Pco2 were much lower in Slc26a4 null relative to wild-type mice due to reduced urinary buffering of secreted H+ by HCO3−. Abundance of non-A, but not type A intercalated cells, was reduced within the cortical collecting ducts of Slc26a4 null mice. Moreover, kidneys from Slc26a4 null mice had reduced H+-ATPase, NBC3 and RhBG total protein expression, particularly within type B and non-A, non-B intercalated cells, although RhCG protein expression was unchanged. Reduced intercalated cell H+/OH− transporter expression is observed in Slc26a4 null mice, which likely attenuates the rise in intracellular and systemic pH expected with genetic disruption of Slc26a4.

scholarly journals Endogenous Endothelins Mediate Increased Acidification in Remnant Kidneys

2001 ◽  
Vol 12 (9) ◽  
pp. 1826-1835
Author(s):  
DONALD E. WESSON
Keyword(s):  
Base Excess ◽  
Left Kidney ◽  
Acid Excretion ◽  
Dietary Acid ◽  
Distal Tubules ◽  
Excretion Rates ◽  
Urinary Acid ◽  
And Control ◽  
Net Acid Excretion

Abstract. Because endothelins (ET) mediate increased renal acidification induced by dietary acid and animals with reduced renal mass exhibit increased urinary ET-1 excretion, the hypothesis that ET mediate increased renal acidification in remnant kidneys was tested. Four weeks before the study, rats underwent a 5/6 nephrectomy (Nx) and a microdialysis apparatus was inserted into the remnant left kidney and the left kidney of sham-treated control animals, for measurements of renal ET-1 contents. Nx animals exhibited greater ET-1 addition to the renal dialysate than did control animals (681 ± 91 versus 290 ± 39 fmol/g kidney wt per min, P < 0.002) and greater urinary ET-1 excretion (346 ± 79 versus 125 ± 24 fmol/d, P < 0.02). Urinary net acid excretion rates were similar for Nx and control animals (732 ± 106 versus 1005 ± 293 μEq/d, P = 0.4), but Nx animals exhibited greater in situ HCO3- reabsorption in proximal (972.3 ± 77 versus 482.6 ± 42.4 pmol/min, P < 0.001) and distal (62.7 ± 6.7 versus 24.3 ± 2.5 pmol/min, P < 0.001) tubules. Orally administered bosentan, an ETA/B receptor antagonist, decreased urinary net acid excretion in Nx animals (to 394 ± 99 μEq/d, P < 0.04 versus without bosentan); the decrease was mediated by decreased HCO3- reabsorption in both the proximal and distal tubules. Furthermore, bosentan decreased blood base excess in Nx animals (0.1 ± 0.3 to -0.12 ± 0.03 μM/ml blood, P < 0.002), consistent with acid retention. The data demonstrate that endogenous ET mediate increased urinary acid excretion in the remnant kidneys of Nx animals.

scholarly journals Effect of growth hormone on renal and systemic acid-base homeostasis in humans

1998 ◽  
Vol 274 (4) ◽  
pp. F650-F657 ◽  
Author(s):  
Anita Sicuro ◽  
Katia Mahlbacher ◽  
Henry N. Hulter ◽  
Reto Krapf
Keyword(s):  
Growth Hormone ◽  
Metabolic Acidosis ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Normal Subjects ◽  
Acid Excretion ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Net Acid Excretion

The effects of recombinant human growth hormone (GH, 0.1 U ⋅ kg body wt−1 ⋅ 12 h−1) on systemic and renal acid-base homeostasis were investigated in six normal subjects with preexisting sustained chronic metabolic acidosis, induced by NH4Cl administration (4.2 mmol ⋅ kg body wt−1 ⋅ day−1). GH administration increased and maintained plasma bicarbonate concentration from 14.1 ± 1.4 to 18.6 ± 1.1 mmol/l ( P < 0.001). The GH-induced increase in plasma bicarbonate concentration was the consequence of a significant increase in net acid excretion that was accounted for largely by an increase in renal [Formula: see text]excretion sufficient in magnitude to override a decrease in urinary titratable acid excretion. During GH administration, urinary pH increased and correlated directly and significantly with urinary[Formula: see text] concentration. Urinary net acid excretion rates were not different during the steady-state periods of acidosis and acidosis with GH administration. Glucocorticoid and mineralocorticoid activities increased significantly in response to acidosis and were suppressed (glucocorticoid) or decreased to control levels (mineralocorticoid) by GH. The partial correction of metabolic acidosis occurred despite GH-induced renal sodium retention (180 mmol; gain in weight of 1.8 ± 0.2 kg, P< 0.005) and decreased glucocorticoid and mineralocorticoid activities. Thus GH (and/or insulin-like growth factor I) increased plasma bicarbonate concentration and partially corrected metabolic acidosis. This effect was generated in large part by and maintained fully by a renal mechanism (i.e., increased renal NH3 production and[Formula: see text]/net acid excretion).

Sign in / Sign up

Export Citation Format

Share Document