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PubMed1991

Distal tubule bicarbonate reabsorption during rebound metabolic alkalosis.

Rebound metabolic alkalosis is a transient alkalemia that is seen during recovery from NH4Cl-induced metabolic acidosis. The persistent elevation of plasma bicarbonate concentration is the result of continuing excretion of net acid by the kidney. Bicarbonate transport by inner medullary collecting ducts has been reported by others to proceed normally (i.e., bicarbonate reabsorption continues in this segment) during rebound metabolic alkalosis. No other segmental responses have been evaluated. Since the surface distal tubule of the rat is known to both reabsorb and secrete bicarbonate in vivo, it was of interest to determine the response of this segment. Our results show that the distal tubule microperfused in vivo during rebound metabolic alkalosis continues to reabsorb significant amounts of bicarbonate, despite the presence of systemic alkalemia that we have previously shown to be associated with distal tubule bicarbonate secretion.

Absorption↗
PubMed1983

Acute respiratory alkalosis and acidosis and rabbit intestinal ion transport in vivo.

The effects of acute respiratory alkalosis and acidosis on electrolyte transport in the rabbit ileum, colon, and gallbladder were studied. During in situ perfusion, anesthetized animals were ventilated with 0, 3, or 8% CO2 gas, creating states of alkalosis (pH 7.49 +/- 0.01, PCO2 = 27.0 +/- 0.9 mmHg, HCO3 = 21.7 mM), normocapnia (pH 7.38 +/- 0.02, PCO2 = 41.3 +/- 1.1 mmHg, HCO3 = 25.9 +/- 0.4 mM), and acidosis (pH 7.21 +/- 0.01, PCO2 = 66.3 +/- 1.3 mmHg, HCO3 = 28.1 +/- 0.8 mM). In the ileum alkalosis decreased the net absorption of water (-36%), sodium (-44%), and chloride (-27%), whereas acidosis had the opposite effect on water (+69%), sodium (+98%), and chloride (+32%) absorption and reduced bicarbonate secretion. Small changes in net potassium absorption occurred in the direction of water movement. There was no effect on the ileal transmural potential difference (PD). The colon and gallbladder did not respond to the acid-base disorders with changes in electrolyte transport or PD. These results suggest that systemic pH and/or PCO2 affect an electroneutral sodium chloride absorptive process in the rabbit ileum. The simple presence of this absorptive process in the gallbladder was not a sufficient basis for this organ to respond to alterations in systemic pH.

Acidosis, Respiratory↗
PubMed1975

Distribution of H+ and HCO3 minus between CSF and blood during respiratory alkalosis in dogs.

Anesthetized, paralyzed dogs after a control period at normal pHa were hyperventilated to produce a hypocapnic alkalosis. The pH, PCO2, (HCO3 minus), and (lactate) in cisternal and lumbar CSF and arterial blood were determined at normal conditions (control) shortly after induction of respiratory alkalosis (time 0) and 3, 4.5, and 6 h thereafter. These values along with measurements of the CSF/plasma DC potential (E) allowed calculations of the electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus. After 6 h of hypocapnic alkalosis, muH+ and muHCO3 minus had returned to minus 0.7 and minus 1.0 mV of control at the cistern and to minus 1.0 and +0.4 mV of control for lumbar CSF. This return of mu is compatible with a passive distribution of these ions though active ion regulation is not ruled out. Assuming passive distribution, differences in deltaE/DELTApHa between metabolic and respiratory acid-base changes determined the extent of CSF pH homeostasis during compensated acid-base derangements.

Acid-Base Equilibrium↗
PubMed1988

Potassium-depletion alkalosis in the rat.

Studies were performed to investigate the role of concomitant chloride depletion in potassium-depletion alkalosis in the rat and the relationship between potassium depletion, plasma bicarbonate (PHCO3), and net acid excretion. 1) Selective potassium depletion (K-DEPL), potassium plus chloride depletion (KCl-DEPL), or selective chloride depletion (Cl-DEPL) was produced by administering a selectively potassium-, potassium and chloride-, or selectively chloride-deficient diet. In K-DEPL and KCl-DEPL rat, PHCO3 increased progressively and similarly during a 38-day period of restriction, whereas net acid excretion was similar and not elevated in either group. Cl-DEPL did not result in alkalosis. Chloride administration without potassium in alkalotic KCl-DEPL rats did not result in a sustained significant decrease in PHCO3. Potassium administration without chloride in alkalotic KCl-DEPL rats decreased PHCO3. Thus concomitant chloride depletion plays a minimal role in the alkalosis produced by dietary-induced potassium depletion. 2) Administration of a chronic acid load to alkalotic K-DEPL rats did not decrease PHCO3, and net acid excretion increased similarly as in normals. In K-DEPL rats after PHCO3 was reduced toward normal levels with acetazolamide, net acid excretion increased sharply above base-line values and PHCO3 increased markedly. Thus the alkalotic K-DEPL rat maintains the ability to excrete a chronic acid load, and a reduction in PHCO3 elicits an increase in acid excretion to restore the initial acid-base condition. These studies suggest that potassium depletion alters the set-point at which the kidney maintains PHCO3.

Acetazolamide↗
PubMed1994

Distal tubule unidirectional HCO3 reabsorption in vivo during acute and chronic metabolic alkalosis in the rat.

During metabolic alkalosis (MA) associated with 2 days of dietary chloride restriction, there is net bicarbonate secretion by rat distal tubules in vivo, whereas after 5 wk of chloride depletion alkalosis there is net bicarbonate reabsorption. To examine unidirectional components of net bicarbonate reabsorption during chronic MA, we measured distal tubule unidirectional bicarbonate secretion (Jsec) and reabsorption (Jreab), as well as the inhibitor sensitivity of Jreab. In control, 2-day, and 7-day alkalosis, Jsec was similar. Jreab, however, was only present in 7-day MA (17 +/- 3 pmol.min-1.mm-1, P < 0.05). This Jreab was completely suppressed by perfusion with 10(-7) M bafilomycin A1, partially suppressed with 10(-5) M Schering (Sch)-28080 (4 +/- 2 pmol.min-1.mm-1, P < 0.1), and converted into a secretory flux by 3 mM amiloride. We conclude that adaptation to chloride depletion MA from the acute secretory phase to the chronic state, where plasma bicarbonate is sustained at elevated levels, does not involve suppression of distal tubule Jsec but rather enhanced Jreab, which is sensitive to bafilomycin, Sch-28080, and amiloride.

Absorption↗
PubMed1995

Effects of chronic Cl depletion alkalosis on proximal tubule transport and renal production of ammonium.

The role of renal ammonium excretion in the maintenance of chronic metabolic alkalosis is poorly defined, particularly under conditions in which the alkalosis is associated with secondary potassium depletion. Therefore, free-flow micropuncture experiments were performed to examine the effects of chronic chloride depletion metabolic alkalosis (CDAlk) on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule (PCT) ammonium transport in the rat in vivo. CDAlk was generated by peritoneal dialysis against NaHCO3 and maintained for 6-7 days by dietary Cl- restriction. Pair-fed controls were dialyzed against NaCl. Rats with CDAlk had elevated plasma HCO3- concentration, hypokalemia, and hypochloremia. HCO3- excretion was negligible in both control and CDAlk rats. Glomerular filtration rate and urine pH did not differ. CDAlk reduced urinary ammonium excretion by 35% but had no significant effect on whole kidney ammonium production. Net secretion of ammonium by the PCT was decreased by 70% and absolute delivery of ammonium out of the PCT was decreased by 55% in the CDAlk rats. The decrease in PCT ammonium secretion was the combined result of a decrease in net ammonium secretion along the early PCT and an increase in net ammonium absorption along the late PCT.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1975

CSF bicarbonate regulation in respiratory acidosis and alkalosis.

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.

Acetazolamide↗
PubMed1982

Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat.

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.

Alkalosis↗
PubMed1983

Changes in brain ECF pH during metabolic acidosis and alkalosis: a microelectrode study.

We used pH-sensitive double-barreled microelectrodes to measure brain extracellular fluid (ECF) pH in anesthetized dogs during isocapnic infusion acidosis (HCl) and alkalosis (Na2CO3) of 45-60 min duration. The diameter of the tips of these electrodes varied from less than 1 to 27 micron and were placed 5 mm below the surface of the parietal cortex. In group I (metabolic acidosis, n = 5) mean plasma and brain ECF pH fell significantly by 0.221 and 0.025, respectively, with changes in brain ECF pH being 11.3% of those noted in plasma. In group II (metabolic alkalosis, n = 5) mean plasma and brain ECF pH rose significantly by 0.170 and 0.049, respectively, with changes in brain ECF pH being 28.8% of those noted in plasma. Mean arterial and sagittal venous PCO2 and cisternal cerebrospinal fluid (CSF) acid-base variables did not change significantly during acid or base infusion. We conclude that during transients of isocapnic metabolic acid-base perturbations ionic gradients exist between brain ECF and CSF and that changes in brain ECF pH measured by microelectrodes follow the changes in plasma pH. These pH changes may play an important role in respiratory adaptations of acute metabolic acidosis and alkalosis.

Acidosis↗
PubMed1984

Ventilatory response to chronic metabolic acidosis and alkalosis in the dog.

Systematic data are not available with regard to the anticipated appropriate responses of arterial PCO2 to primary alterations in plasma bicarbonate concentration. In the present study, we attempted to rigorously characterize the ventilatory response to chronic metabolic acid-base disturbances of graded severity in the dog. Animals with metabolic acidosis produced by prolonged HCl feeding and metabolic alkalosis of three different modes of generation, i.e., diuretics (ethacrynic acid or chlorothiazide), gastric drainage, and administration of deoxycorticosterone acetate (alone or in conjunction with oral sodium bicarbonate), were examined. The results indicate the existence of a significant and highly predictable ventilatory response to chronic metabolic acid-base disturbances. Moreover, the magnitude of the ventilatory response appears to be uniform throughout a wide spectrum of chronic metabolic acid-base disorders extending from severe metabolic acidosis to severe metabolic alkalosis; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin. Furthermore, the data suggest that the ventilatory response to chronic metabolic alkalosis is independent of the particular mode of generation.

Acidosis↗
PubMed1986

Ventilatory acclimatization to hypoxia is not dependent on cerebral hypocapnic alkalosis.

We previously demonstrated that, in awake goats, 6 h of hypoxic carotid body perfusion during systemic normoxia produced time-dependent hyperventilation that is typical of ventilatory acclimatization to hypoxia (VAH). The hypocapnic alkalosis that occurred could have produced VAH by inducing cerebral vasoconstriction and brain lactic acidosis even though systemic arterial normoxia was maintained. In the present study we tested the hypothesis that hypocapnic alkalosis is a necessary component of VAH. Goats were prepared so that one carotid body could be perfused, from an extracorporeal circuit, with blood in which gas tensions could be controlled independently from the blood perfusing the systemic arterial system, including the brain. Using this preparation we carried out 4 h of hypoxic carotid body perfusion while maintaining systemic arterial (and brain) normoxia in awake goats. Expired minute ventilation (VE) was measured while CO2 was added to inspired air to maintain normocapnia. Carotid body PCO2 and PO2 were maintained near 40 Torr during the 4-h carotid body perfusion. Control mean VE was 8.65 +/- 0.48 l/min (mean +/- SE). With acute carotid body hypoxia (30 min) VE increased to 21.73 +/- 2.02 l/min (P less than 0.05); over the ensuing 3.5 h of carotid body hypoxia, VE progressively increased to 39.14 +/- 4.14 l/min (P less than 0.05). These data indicate that neither cerebral hypoxia nor hypocapnic alkalosis are required to produce VAH. After termination of the 4-h carotid body stimulation, hyperventilation was not maintained in these studies, i.e., there was no deacclimatization. This suggests that acclimatization and deacclimatization are produced by different mechanisms.

Acclimatization↗
PubMed2002

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P < 0.05) because of hyperventilation (arterial PCO2 25.6 +/- 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

Aldosterone↗
PubMed2001

Evaluation of subcutaneous tissue gases and pH during induction of acidosis and alkalosis. An experimental study in pigs.

Peripheral tissue oxygen utilization was studied during hypoxic-induced acidosis and sodium bicarbonate-induced alkalosis in 8 domestic pigs by measurements of subcutaneous oxygen tension (PscO2), carbon dioxide tension (PscCO2) and pH (pH(sc)) in relation to central hemodynamic parameters and oxygenation. Hypoxic-induced acidosis resulted in a decrease in P(sc)O(2) [corrected] and arterial oxygen tension (P(a)O(2)) to one third of baseline values (p < 0.05), an increase in PscCO2 and arterial carbon dioxide tension (PaCO2) from 41 to 55 and 34 to 39 mm Hg, respectively (p < 0.05), and a decrease in pH(sc) from 7.47 to 7.30 (p < 0.05). PscO2 and PaO2 increased during reversal of hypoxia and infusion of bicarbonate (p < 0.05), without reaching baseline values. In parallel PscCO2 decreased and pH(sc) increased but changes lagged behind changes in blood gases. Alkalosis established by further infusion of bicarbonate resulted in a decrease in PaO2 to 62 mm Hg whereas PscO2 remained below baseline values (p < 0.05). Correction of oxygen utilization in the subcutaneous tissue as measured by the markers PscCO2 and pH(sc) is slower than indicated by changes in tissue oxygen tension, blood gases and pH. Overcompensation of acidosis with bicarbonate resulting in alkalosis impairs oxygenation.

Acidosis↗
PubMed1991

Hypoventilation in a dialysis patient with severe metabolic alkalosis: treatment by hemodialysis.

A patient with end-stage renal disease (ESRD) developed metabolic alkalosis and alkalemia from protracted vomiting. As a result of the absence of the alkali excretory capacity in this patient with ESRD, the alkaline load accumulated rapidly. Once the amount of acid lost from vomiting exceeded the amount of acid gained from metabolism, alkalemia supervened. The initial arterial blood gas on room air revealed hypercarbia, hypoxia and alkalemia. Her serum bicarbonate was greater than 50 mEq/l. Compensatory hypoventilation occurred. In this report, the extent of compensatory hypoventilation in the setting of metabolic alkalosis in patients treated for ESRD and therapeutic approaches to this problem will be discussed. Treatment was aimed at correcting the primary disorder, namely metabolic alkalosis. Conventional bicarbonate dialysis was shown to be effective in improving acid-base homeostasis in this patient.

Alkalosis↗
PubMed1986

Studies on therapy of metabolic alkalosis during experimental uremia. Influences of arginine-hydrochloride on the intra- and extracellular acid-base status of the rat.

Severe metabolic alkalosis, combined with acute renal failure or uremia presents a difficult problem for the clinician. The standard treatment modalities of metabolic alkalosis are then limited and infusion of arginine-HCl is often tried in these cases. It was the purpose of this investigation to study the effects of arginine-HCl on the whole-body acid-base status during experimental uremia. While the extracellular acid-base status was determined from blood-gas measurements, the intracellular pH was calculated from the distribution of 5,5-dimethyl-2,4-oxazolidinedione. It was found that administration of arginine-HCl leads to a significant increase of intracellular pH though extracellular plasma pH decreases, and that arginine-HCl causes only an insignificant reduction of the intracellular bicarbonate concentration. The observed intracellular pH increase may have adverse consequences for patients and raises objections to the further use of arginine-HCl in the treatment of metabolic alkalosis, especially during renal failure or uremia.

Acid-Base Equilibrium↗
PubMed1994

Quantitative cerebrospinal fluid acid-base balance in acute respiratory alkalosis.

Data on canine cisternal cerebrospinal fluid (CSF) ions in acute respiratory alkalosis are limited and fragmentary. We hypothesized that with the fall in arterial PCO2 (PaCO2) and in the face of normal osmoregulation, CSF [Na+] remains relatively constant and CSF [Na+-Cl-] narrows to account in part for the fall in CSF [HCO3-]. We therefore measured blood and CSF acid-base variables and ions of two groups of pentobarbital-anesthetized, mechanically ventilated dogs (n = 10 in each group). In the control group, PaCO2 was kept constant and changes in serum and CSF ions were minimal. In Group II (acute respiratory alkalosis), both PaCO2 and cisternal CSF PCO2 decreased by 10 mm Hg. Five hours after induction of respiratory alkalosis, mean CSF [HCO3-] decreased significantly by 4.4 +/- 1.2 mEq/L (mean +/- SD). The fall in CSF [HCO3-] was similar to changes in CSF strong ion difference (SID = Na(+)+K(+)+Ca(2+)+Mg(2+)-CL(-)-lactate), which decreased 4.4 +/- 1.9 mEq/L. Concentrations of the four major CSF cations did not change significantly. Cisternal CSF lactate rose significantly by 1.2 +/- 0.9 mEq/L, accounting for 25% of the change in CSF [HCO3-]. The remaining (75%) change in CSF [HCO3-] was accounted for by changes in CSF [Cl-].

Acid-Base Equilibrium↗
PubMed1983

Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.

Studies were undertaken to define the pattern of proximal tubular bicarbonate reabsorption and its relation to tubular and capillary PCO2 in rats with chronic metabolic alkalosis (CMA). CMA was induced by administering furosemide to rats ingesting a low electrolyte diet supplemented with NaHCO3 and KHCO3. Proximal tubular bicarbonate reabsorption and PCO2 were measured in CMA rats either 4-7 or 11-14 d after furosemide injection, in order to study a wide range of filtered bicarbonate loads. A group of nine age-matched control animals, fed the same diet but not given furosemide, was studied for comparison. In a third group of controls, the filtered load of bicarbonate was varied over the same range as in the CMA rats by plasma infusion and aortic constriction. The CMA rats had significant alkalemia and hypokalemia (4-7 d: pH 7.58, HCO3 38.3 meq/liter, K+ 2.1 meq/liter; 11-14 d: pH 7.54, HCO3 38.1 meq/liter, K+ 2.5 meq/liter). Nonetheless, proximal bicarbonate reabsorption was not significantly different from that seen in control rats at any given load of filtered bicarbonate (from 250 to 1,300 pmol/min). In both control and CMA rats, 83-85% of the filtered bicarbonate was reabsorbed by the end of the accessible proximal tubule. These observations indicate that proximal bicarbonate reabsorption is determined primarily by the filtered load in chronic metabolic alkalosis. When single nephron glomerular filtration rate (SNGFR) is reduced by volume depletion in the early postfurosemide period, the filtered load and the rate of proximal bicarbonate reabsorption remain at or below control levels, maintaining metabolic alkalosis. In the late postfurosemide period, however, SNGFR returned to control levels in some instances. In these animals, both the filtered load and rate of proximal reabsorption were increased above the highest levels seen in control animals. The PCO2 gradient between the peritubular capillaries and arterial blood (Pc-Art) was significantly higher in CMA than in control, even though the rate of proximal bicarbonate reabsorption did not differ. Thus, proximal bicarbonate reabsorption did not appear to be the primary determinant of Pc-Art PCO2. PCO2 in the early proximal (EP) tubule was significantly higher than in either the late proximal (LP) tubule or peritubular capillaries in both control and CMA rats. The EP-LP PCO2 gradient correlated directly with proximal bicarbonate reabsorption (P less than 0.05). The small elevation in PCO2 in EP may be related to CO2 generated at this site in the process of bicarbonate reabsorption.

Absorption↗
PubMed1989

Augmented bicarbonate reabsorption by both the proximal and distal nephron maintains chloride-deplete metabolic alkalosis in rats.

Whether augmented bicarbonate reabsorption by renal tubular epithelium contributes to the maintenance of chloride-deplete metabolic alkalosis is not clear. This study used free-flow micropuncture to investigate bicarbonate reabsorption by surface nephron segments in a rat model of diuretic-induced alkalosis compared to control. The proximal and distal nephron of the alkalotic animals had higher values for both delivered load to and absolute reabsorption from these segments. The proximal tubules of alkalotic and control animals had similar values for the slopes of the linear regression of delivered load vs. reabsorption and for the bicarbonate tubular fluid to plasma (TF/P) ratio at the late proximal tubule. By contrast, the corresponding analysis for the distal segment of alkalotic animals revealed a greater slope (0.98 vs. 0.81, P less than 0.003) and a smaller bicarbonate TF/P ratio at the late distal tubule (0.10 vs. 0.16, P less than 0.006). The data indicate that augmented bicarbonate reabsorption by both the proximal and distal nephron contributes to maintaining the alkalosis of this model. The data suggest primary stimulation of bicarbonate reabsorption in the distal nephron and load-dependent reabsorption in the proximal tubule.

Absorption↗