scholarly journals Expression of rat thick limb Na/H exchangers in potassium depletion and chronic metabolic acidosis

2001 ◽  
Vol 60 (4) ◽  
pp. 1386-1396 ◽  
Author(s):  
Kamel Laghmani ◽  
Christine Richer ◽  
Pascale Borensztein ◽  
Michel Paillard ◽  
Marc Froissart
Keyword(s):  
Metabolic Acidosis ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of potassium depletion during chronic metabolic acidosis in the rat

1987 ◽  
Vol 252 (1) ◽  
pp. F122-F130 ◽  
Author(s):  
J. D. Scandling ◽  
D. B. Ornt
Keyword(s):  
Metabolic Acidosis ◽  
Fractional Excretion ◽  
Potassium Depletion ◽  
Urinary Flow ◽  
Aldosterone Secretion ◽  
Chronic Metabolic Acidosis ◽  
Base Disorder ◽  
Urinary Potassium ◽  
K Depletion ◽  
Isolated Kidneys

Pair-fed rats on a normal K diet were given either 1.5% NH4Cl or water for 4 days. The acid-fed animals developed metabolic acidosis, negative K balance, and K depletion. Urinary Na excretion and urinary flow were not different between the groups beyond the first day. After the 4 days, isolated kidneys from animals in each of these groups were perfused at normal pH and bicarbonate concentrations. Urinary K excretion was similar between the groups despite the potassium depletion in the acid-fed animals. In contrast, isolated kidneys from animals with comparable K depletion induced by dietary K restriction readily conserved K (fractional excretion 0.35 +/- 0.04 vs. 0.83 +/- 0.09 by the kidneys from acid-fed animals, P less than 0.01). Sodium excretion and urinary flow were similar among the three groups of isolated kidneys. Plasma aldosterone concentrations were greater in the acid-fed rats after the 4 days of NH4Cl ingestion than in the control animals (43 +/- 10 vs. 10 +/- 2 ng/dl, P less than 0.01). Adrenalectomized rats were treated with either normal (4 micrograms/day) or high (22 micrograms/day) aldosterone replacement while ingesting NH4Cl for 4 days. Only in the presence of high aldosterone replacement did the acid-fed adrenalectomized animals develop K depletion. We conclude that chronic metabolic acidosis stimulates aldosterone secretion, and that aldosterone maintains the inappropriately high urinary potassium excretion and K depletion seen in this acid-base disorder.

The Effect of Chronic Metabolic Acidosis on the End Organ Responsiveness to Parathyroid Hormone in Man*

1983 ◽  
Vol 56 (3) ◽  
pp. 619-622 ◽  
Author(s):  
JEFFREY A KRAUT ◽  
EARL M. GORDON ◽  
JOHN C. RANSOM ◽  
JACK W. COBURN ◽  
KIYOSHI KUROKAWA
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Chronic Metabolic Acidosis

Basolateral membrane H-OH-HCO3 transport in the proximal tubule

1989 ◽  
Vol 256 (5) ◽  
pp. F751-F765
Author(s):  
P. A. Preisig ◽  
R. J. Alpern
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Respiratory Acidosis ◽  
Cell Voltage ◽  
Transport Mechanisms ◽  
Transport Capacity ◽  
Chronic Metabolic Acidosis

This review focuses on the basolateral membrane mechanisms of H-OH-HCO3 transport in the proximal tubule. The mechanism that has the greatest transport capacity and mediates most of transepithelial H-HCO3 transport is the electrogenic, Na-3HCO3 cotransporter. This transporter has been extensively characterized in the salamander, rat, and rabbit proximal tubule, and has now been found in a number of other epithelia that effect transepithelial NaHCO3 transport. Transporter rate is sensitive to intra- and extracellular [Na], intra- and extracellular [HCO3]/pH, and cell voltage. Adaptations in transporter activity have been demonstrated in chronic metabolic acidosis and alkalosis, chronic respiratory acidosis and alkalosis, and chronic hyperfiltration. In addition to the Na-3HCO3 cotransporter, the basolateral membrane possesses both Na-dependent and -independent Cl-HCO3 exchangers, a H leak, and in the S3 proximal tubule an Na-H antiporter. The role of these H-OH-HCO3 transport mechanisms in transcellular HCO3 and Cl absorption and pHi defense is discussed.

Inhibition of 25-hydroxyvitamin D3-1-hydroxylase by chronic metabolic acidosis

1982 ◽  
Vol 243 (4) ◽  
pp. E265-E271
Author(s):  
G. S. Reddy ◽  
G. Jones ◽  
S. W. Kooh ◽  
D. Fraser
Keyword(s):  
Vitamin D ◽  
Metabolic Acidosis ◽  
Rat Kidney ◽  
Ion Concentration ◽  
Hydroxylase Activity ◽  
Renal Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Hydrogen Ion Concentration ◽  
Chronic Metabolic Acidosis ◽  
Negative Linear Correlation

Chronic metabolic acidosis had been shown to influence the renal metabolism of 25-hydroxyvitamin D3. Using the isolated perfused rat kidney model, we evaluated the rates of synthesis of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in vitamin D-depleted [D(-)] and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] in vitamin D-replete [D(+)] rats. Metabolic acidosis was induced in both groups of rats by feeding aqueous ammonium chloride for 9 days. Kidneys isolated from D(-) acidotic rats (mean pH, 7.11) exhibited a decreased rate of 1,25(OH)2D3 synthesis (0.79 +/- 0.17 pmol produce . h-1 . g kidney-1) when compared with that (1.27 +/- 0.09) of D(-) nonacidotic (mean pH, 7.33) rats. There was a significant negative linear correlation between the rate of synthesis of 1,25(OH)2D3 and the hydrogen ion concentration of the animal (r = 0.79, P less than 0.005). The rate of synthesis of 24,25(OH)2D3 by the kidneys from D(+) acidotic (mean pH, 7.06) and nonacidotic (mean pH, 7.39) rats did not differ (0.81 +/- 0.21 vs. 0.60 +/- 0.12 pmol product . h-1 . g kidney-1). It is concluded that chronic acidosis suppressed 1-hydroxylase activity, but does not suppress 24-hydroxylase activity.

Effect of chronic metabolic acidosis on net electrolyte transport in rat colon

1989 ◽  
Vol 256 (6) ◽  
pp. G1036-G1040 ◽  
Author(s):  
G. M. Feldman
Keyword(s):  
Metabolic Acidosis ◽  
Distal Colon ◽  
Distal Segment ◽  
Proximal Colon ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Chronic Metabolic Acidosis ◽  
In Situ Perfusion ◽  
Arterial Blood ◽  
Acute Correction

Rats fed NH4Cl (5 meq.100 g body wt-1.day-1) for one week developed chronic metabolic acidosis and had an arterial blood pH and plasma HCO3- concentration of 7.27 +2- 0.02 and 16.2 +/- 0.8 meq/l, respectively; control animals had values of 7.36 +/- 0.01 and 22.4 +/- 0.5 meq/l, respectively. Net electrolyte transport was measured in proximal and distal colonic segments by in situ perfusion. In proximal colon, chronic metabolic acidosis increased HCO3- absorption from 3.3 +/- 0.8 to 6.4 +/- 0.6 mu eq.min-1.g-1 but did not alter Na+ absorption. In distal colon, although Na+ transport was unaffected, chronic acidosis reduced HCO3- secretion from -6.9 +/- 0.8 to -4.4 +/- 0.7 mu eq.min-1.g-1 and increased voltage from -18.9 +/- 2.0 to -51.1 +/- 4.2 mV. To evaluate the dependence of these effects on altered arterial pH and HCO3- concentration, NaHCO3 was infused intravenously, raising pH and HCO3- concentration to 7.53 +/- 0.04 and 23.9 +/- 1.7 meq/l, respectively. Although acute correction of chronic metabolic acidosis reduced HCO3- absorption in proximal colon, it did not affect HCO3- secretion or voltage in the distal segment, suggesting that proximal and distal colon respond differently to chronic metabolic acidosis. These results also suggest that chronic metabolic acidosis alters the mechanisms of ion transport in distal colon.

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