Effect of potassium depletion and protein intake in vivo on renal tubular bicarbonate transport in vitro

1987 ◽  
Vol 252 (3) ◽  
pp. F509-F516 ◽  
Author(s):  
T. D. McKinney ◽  
K. K. Davidson
Keyword(s):  
Potassium Depletion ◽  
Co2 Absorption ◽  
Urine Ph ◽  
Outer Medulla ◽  
Acid Urine ◽  
Arterial Blood ◽  
Blood Ph ◽  
Renal Tubular ◽  
Collecting Tubules

These studies evaluated the effect of decreased dietary potassium and increased dietary protein content in rabbits on systemic acid-base parameters, urine pH, and segmental renal tubular bicarbonate handling in vitro. Animals fed a potassium-deficient high-protein diet (KD) for 2 wk developed metabolic acidosis (arterial blood pH 7.31 vs. 7.43) and excreted a more acid urine than control animals fed a diet with normal amounts of potassium and protein; whereas, animals fed the same potassium deficient diet to which supplemental potassium was added (KD + K+) excreted an even more acid urine and had a blood pH of 7.36. In superficial proximal convoluted and straight tubules, there were no differences in rates of fluid and total CO2 absorption between control and KD tubules. Cortical collecting tubules obtained from KD and KD + K+ animals absorbed, and control tubules secreted total CO2 in vitro. With an ambient potassium concentration of 2.5 mM, collecting tubules obtained from the inner stripe of the outer medulla of KD animals absorbed significantly less total CO2 than control tubules. The same tendency was observed in collecting tubules from the outer stripe of the outer medulla. Plasma aldosterone levels fell with development of potassium depletion. Administration of deoxycorticosterone for 1 day to KD animals was associated with a lower urine pH and higher arterial blood pH than in untreated KD animals and with increased total CO2 absorption by both cortical collecting tubules and tubules from the inner stripe of the outer medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of respiratory acidosis on HCO3- transport by rabbit collecting tubules

1988 ◽  
Vol 255 (4) ◽  
pp. F656-F665 ◽  
Author(s):  
T. D. McKinney ◽  
K. K. Davidson
Keyword(s):  
Calcium Concentration ◽  
Basolateral Membrane ◽  
Respiratory Acidosis ◽  
Bicarbonate Transport ◽  
Co2 Absorption ◽  
Distal Nephron ◽  
Outer Medulla ◽  
Collecting Tubules ◽  
Stimulation Of

These studies were performed to determine whether in vitro elevation of bath PCO2 with associated reduction in pH (acute respiratory acidosis) affected bicarbonate transport by isolated perfused rabbit cortical collecting tubules (CCT) and collecting tubules from the outer (OMCTos) and inner (OMCTis) stripes of the outer medulla. When the PCO2 was elevated and pH reduced from approximately 7.4 to 7.0 the rate of total CO2 absorption increased to 252% of that observed at pH 7.4 in CCT, 146% in OMCTos, and 150% in OMCTis. In OMCTis, pretreatment with colchicine inhibited the stimulation of total CO2 absorption associated with respiratory acidosis, whereas lumicolchicine did not. Similar inhibition was observed in the presence of maptam and a low calcium concentration and in the presence of a calmodulin inhibitor. No differences were observed in apical or basolateral membrane morphometry of principal or intercalated cells between control tubules and those subjected to respiratory acidosis. The results indicate that acute respiratory acidosis stimulates acidification by the rabbit distal nephron in vitro through a process(es) that, at least in OMCTis, evidently involves the cell cytoskeleton and changes in cell calcium and calmodulin activities.

Bicarbonate transport in collecting tubules from outer stripe of outer medulla of rabbit kidneys

1987 ◽  
Vol 253 (5) ◽  
pp. F816-F822 ◽  
Author(s):  
T. D. McKinney ◽  
K. K. Davidson
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Disulfonic Acid ◽  
Bicarbonate Transport ◽  
Co2 Absorption ◽  
Outer Medulla ◽  
Carbonic Anhydrase Inhibitors ◽  
Outer Stripe ◽  
Collecting Tubules

The purpose of this study is to characterize the features of bicarbonate (total CO2) transport in isolated perfused collecting tubules obtained from the outer stripe of the outer medulla (OMCTos) of rabbit kidneys. Under control conditions (25 mM HCO3- in the perfusate and bath), all OMCTos studied absorbed total CO2 at a mean rate of 8.61 +/- 0.44 pmol.mm-1.min-1. Ouabain (10(-4) M in the bath) did not affect the rate of total CO2 absorption (JtCO2). Addition of the diethylstilbene 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) in a concentration of 10(-4) M or replacement of bath chloride by gluconate reduced JtCO2 by approximately 50%, whereas replacement of luminal chloride increased JtCO2 by 40%. The carbonic anhydrase inhibitors acetazolamide and ethoxyzolamide in concentrations of 10(-4) M had little effect on JtCO2. In a concentration of 10(-3) M, acetazolamide reduced JtCO2 by only 31%. OMCTos obtained from rabbits with ammonium chloride-induced metabolic acidosis did not have increased rates of total CO2 absorption compared with the control, but treatment of animals with mineralocorticoids increased JtCO2. These results indicate that OMCTos are capable of significant bicarbonate absorption in vitro. This absorption 1) is independent of sodium transport, 2) appears to require, at least in large part, HCO3- or OH- -Cl- exchange across the basolateral cell membrane of acid-secreting cells, 3) is much more resistant to inhibition by carbonic anhydrase inhibitors than reported previously for other rabbit nephron segments, and 4) is stimulated by prior mineralocorticoid treatment of animals but not by prior metabolic acidosis in vivo.

Vanadate causes hypokalemic distal renal tubular acidosis

1992 ◽  
Vol 262 (3) ◽  
pp. F449-F453 ◽  
Author(s):  
E. Dafnis ◽  
M. Spohn ◽  
B. Lonis ◽  
N. A. Kurtzman ◽  
S. Sabatini
Keyword(s):  
Renal Tubular Acidosis ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Distal Renal Tubular Acidosis ◽  
Urine Ph ◽  
A Value ◽  
Blood Ph ◽  
Collecting Tubule ◽  
Renal Tubular ◽  
Collecting Tubules

Considerable evidence supports the presence of an H(+)-K(+)-ATPase along the mammalian nephron. Inhibition of this enzyme might be expected to reduce acid excretion while increasing potassium excretion, thus causing hypokalemic distal renal tubular acidosis (RTA). In this study we administered vanadate at a dose of 5 mg/kg ip for 10 days to rats. These animals developed hypokalemic distal RTA with a blood pH of 7.22 +/- 0.01, a plasma bicarbonate of 15.2 +/- 0.6 meq/l, and a plasma potassium of 3.28 +/- 0.06 meq/l. The vanadate-treated animals had a urine pH of 6.70 +/- 0.09, a value significantly higher than NH4Cl-treated animals with the same degree of acidemia (urine pH = 5.25 +/- 0.04). When cortical collecting tubules (CCT) from these animals were microdissected and H(+)-K(+)-ATPase was measured, it was decreased by approximately 75% (P less than 0.001); but H(+)-ATPase was no different from control. In medullary collecting tubule, H(+)-K(+)-ATPase was also decreased but less than in CCT. Muscle potassium concentration in the vanadate-treated animals was significantly lower than in controls. These results demonstrate that vanadate causes hypokalemic distal RTA in association with inhibition of collecting tubule H(+)-K(+)-ATPase activity.

Effect of acid lumen pH on potassium transport in renal cortical collecting tubules

1976 ◽  
Vol 230 (1) ◽  
pp. 239-244 ◽  
Author(s):  
JF Boudry ◽  
LC Stoner ◽  
MB Burg
Keyword(s):  
Mean Value ◽  
Potassium Transport ◽  
Sodium Absorption ◽  
Positive Voltage ◽  
Tubule Lumen ◽  
Potassium Secretion ◽  
Transepithelial Voltage ◽  
Renal Tubular ◽  
Collecting Tubules

In order to determine the effect of acid lumen pH on renal tubular potassium transport, cortical collecting tubules were dissected from rabbit kidneys and perfused in vitro. When the pH of the perfusate was lowered from 7.4 to 6.8, potassium secretion into the tubule lumen decreased by an average of 47%. The transepithelial voltage increased from a mean value of -32 mV (lumen negative) at pH 7.4 to -51 mV at PH 6.8. Net sodium absorption from the tubule lumen was essentially unchanged (5% mean decrease). Transepithelial voltage and potassium secretion returned to control values when the pH of the perfusate was raised to 7.4. Alterations in pH of the bath had no comparable effect on the transepithelial voltage, whether the bath pH was increased or decreased. We conclude that a decrease in the pH of the tubule fluid of itself inhibits active potassium secretion in this tubule segment, providing an additional explanation for the decrease in potassium excretion found in acidosis. The negative voltage (presumably caused by sodium absorption out of the lumen) is increased under these conditions, possibly because of reduction of a smaller counterbalancing positive voltage caused by potassium secretion into the lumen.

Collecting tubule adaptation to respiratory acidosis induced in vivo

1990 ◽  
Vol 258 (1) ◽  
pp. F15-F20 ◽  
Author(s):  
M. E. Laski ◽  
N. A. Kurtzman
Keyword(s):  
Respiratory Acidosis ◽  
In Vitro Study ◽  
Co2 Flux ◽  
Urine Ph ◽  
Collecting Tubule ◽  
Bicarbonate Solutions ◽  
Animal Exposure ◽  
Collecting Tubules

To examine the effects of respiratory acidosis in vivo on the adaptation of acidification in the collecting tubule, New Zealand White rabbits were exposed to a 6.7% CO2-93.3% O2 gas mixture in an environmental chamber for 0, 6, 24, or 48 h before obtaining collecting tubules for in vitro study. These collecting tubules were then perfused and bathed in vitro in identical Krebs-Ringer bicarbonate solutions. After 1 h equilibration total CO2 flux (JtCO2) was measured. The urine pH of the rabbits fell, whereas the blood bicarbonate rose as CO2 exposure time increased. In cortical collecting tubules, JtCO2 in vitro correlated with length of animal exposure to hypercarbia (y = 1.14174 + 0.1437x, r = 0.57, P = 0.002), and with the blood bicarbonate of the animal (y = 26.8471 + 0.0858x, r = 0.59, P less than 0.05). In vitro JtCO2 in medullary collecting tubules from rabbits that had been in hypercarbic atmosphere for 48 h (23.2 +/- 4.9 pmol.mm-1.min-1) did not differ from JtCO2 in control tubules (25.0 +/- 3.2 pmol.mm-1.min-1, not significant). Thus the cortical collecting tubule exhibits an adaptive increase in JtCO2 in response to hypercarbia, whereas the medullary collecting tubule does not.

In vitro effects of pH and hemoglobin-oxygen saturation on plasma and erythrocyte K+ levels in blood from trout

1992 ◽  
Vol 72 (4) ◽  
pp. 1291-1296 ◽  
Author(s):  
O. B. Nielsen ◽  
G. Lykkeboe
Keyword(s):  
Hemoglobin Oxygen Saturation ◽  
Blood Samples ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Arterial Blood ◽  
Blood Ph ◽  
Effects Of Ph ◽  
Net Uptake ◽  
In Vitro Effects ◽  
K Concentration

Plasma and erythrocyte K+ were monitored during storage and tonometry of blood samples taken from resting rainbow trout, Oncorhynchus mykiss. During storage of arterial blood samples, plasma K+ concentration increased by 38% in 12 min. During extended tonometry of blood with a pH near 7.9 and full hemoglobin-bound oxygen (HbO2) saturation the erythrocytes showed a net loss of K+. Plasma K+ concentration increased from 2.9 mM to a near steady-state value of 5.6 mM. When tonometered at a pH near 7.2 and a HbO2 saturation at approximately 4% the erythrocytes took up K+, leading to a dramatic reduction in plasma K+ concentration to 0.2 mM. This net uptake was stimulated by isoprenaline and was inhibited by ouabain. It is concluded that net erythrocyte K+ uptake and loss can be induced in trout by changes in blood pH or HbO2 saturation in vitro.

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)

Renal Tubular Acidosis in a Patient with Recurrent Metabolic Alkalosis

PEDIATRICS ◽  
1983 ◽  
Vol 72 (2) ◽  
pp. 207-210
Author(s):  
Leonard C. Hymes ◽  
Barry L. Warshaw
Keyword(s):  
Renal Tubular Acidosis ◽  
Serum Potassium ◽  
Metabolic Alkalosis ◽  
Failure To Thrive ◽  
Unusual Presentation ◽  
Potassium Depletion ◽  
Type I ◽  
Serum Bicarbonate ◽  
Urine Ph ◽  
Renal Tubular

A 7-month-old infant with failure to thrive and recurrent episodes of vomiting and metabolic alkalosis was evaluated. Urine pH, serum bicarbonate, and urine Pco2-blood Pco2 studies were consistent with the diagnosis of distal renal tubular acidosis (RTA-type I). Analysis of serum potassium and chloride levels during periods of alkalosis and acidosis revealed that potassium depletion and hypochloremic volume contraction served to maintain the alkalotic state despite the presence of an underlying chronic acidosis. This case represents an unusual presentation for renal tubular acidosis and suggests that, under certain conditions, renal tubular acidosis may predispose to the maintenance of a metabolic alkalosis.

Protease effects on adenylate cyclase in potassium-depleted rabbit kidney

1988 ◽  
Vol 255 (5) ◽  
pp. F1033-F1039
Author(s):  
K. H. Raymond ◽  
S. D. Holland ◽  
T. K. Hymer ◽  
T. D. McKinney ◽  
M. S. Katz
Keyword(s):  
Adenylate Cyclase ◽  
Proteolytic Enzymes ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Rabbit Kidney ◽  
Potassium Depletion ◽  
Collecting Tubules ◽  
And Control

Potassium depletion in rabbits induces a renal concentrating defect in vivo and decreased hydrosmotic response to arginine vasopressin (AVP) in isolated cortical collecting tubules (CCT) perfused in vitro. The molecular basis of the AVP resistance in potassium depletion was investigated by comparing AVP-responsive adenylate cyclase activities in CCT from potassium-depleted and control rabbits. Vasopressin-responsive enzyme activity was impaired in CCT dissected from kidneys of potassium-depleted rabbits but not when kidneys were treated with collagenase to improve microdissection conditions. Potassium depletion also depressed parathyroid hormone (PTH)-stimulated adenylate cyclase activity in proximal straight tubules (PST) dissected from untreated but not collagenase-treated kidneys. Commercially available collagenase, which also contains other proteolytic enzymes, increased AVP-sensitive adenylate cyclase activity in control CCT, and trypsin treatment of CCT dissected without collagenase abolished the decrease in AVP-sensitive activity induced by potassium depletion. Inclusion of trypsin inhibitor during collagenase treatment of kidneys lowered AVP response in CCT from potassium-depleted rabbits. These results demonstrate that potassium depletion impairs hormone-sensitive adenylate cyclase of CCT (and PST) by a protease-sensitive mechanism.

Effect of metabolic acidosis on proximal tubular total CO2 absorption

1985 ◽  
Vol 249 (1) ◽  
pp. F62-F68 ◽  
Author(s):  
R. T. Kunau ◽  
J. I. Hart ◽  
K. A. Walker
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Co2 Absorption ◽  
Arterial Blood ◽  
Blood Ph ◽  
In Series ◽  
Proximal Tubular

In vivo microperfusion studies of the proximal convoluted tubule of the rat were performed to determine the effect of metabolic acidosis on total CO2 (tCO2) absorption. In series I, tubular perfusion was performed in control and acidotic rats in a manner by which similar mean total CO2 concentrations in the proximal tubule were maintained. Comparable ranges of perfusion rate were studied in both groups. Following 3 days of HCl ingestion, plasma tCO2 was 20.0 +/- 0.9 mM in the acidotic rats whereas it was 29.6 +/- 0.53 mM in control rats. The arterial blood pH values were 7.25 +/- 0.02 vs. 7.43 +/- 0.01. Starting tCO2 perfusate concentrations were identical in both groups, 29.3 and 29.7 mM, as were the concentrations at the end of the perfused segments, 21.2 and 21.9 mM. The absorption of tCO2 (JtCO2, pmol X mm-1 X min-1) was significantly greater in the acidotic rats than in the controls, 576 +/- 39 vs. 256 +/- 21. At all perfusion rates studied, proximal tubular JtCO2 was higher in the acidotic than in the control rats. In series II, similar lengths of the late proximal tubule were perfused at the same rate in control and acidotic rats. Again, JtCO2 was higher in the acidotic rats, 352 +/- 19 vs. 198 +/- 13. The results indicate that at comparable luminal tCO2 concentration and tubular fluid flow rates, tCO2 absorption is significantly increased in the acidotic state. Although other mechanisms cannot be excluded, the finding of an increase in proximal tCO2 absorption in the acidotic rats is in agreement with the presence of an accelerated Na+/H+ exchange rate in brush border membrane vesicles obtained from the renal cortex of animals with metabolic acidosis.

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