Suppression of distal urinary acidification after recovery from chronic hypocapnia

1983 ◽  
Vol 245 (4) ◽  
pp. F433-F442 ◽  
Author(s):  
D. C. Batlle ◽  
K. Itsarayoungyuen ◽  
M. Downer ◽  
R. Foley ◽  
J. A. Arruda ◽  
...  
Keyword(s):  
Sodium Bicarbonate ◽  
Normal Control ◽  
Hydrogen Ion ◽  
Bicarbonate Concentration ◽  
Urine Ph ◽  
Ion Secretion ◽  
Blood Ph ◽  
Urinary Acidification ◽  
Cell Ph ◽  
Prolonged Duration

This study examined urinary acidification shortly after recovery from chronic hypocapnia induced by hypoxemia. Distal acidification was evaluated by measuring the urinary PCO2 and urine-blood PCO2 difference (U-B PCO2) when blood PCO2 had returned to normal. In posthypocapnic rats, maximal alkalinization of the urine by acute sodium bicarbonate loading failed to increase urine PCO2 and U-B PCO2 to the level of posthypoxemic control rats and normal control rats with comparable blood pH and urine bicarbonate concentration. To test the hypothesis that decreased distal hydrogen ion secretion in posthypocapnic rats resulted from intracellular alkalosis secondary to protracted hypocarbia, posthypocapnic rats were exposed to hypercapnia of brief duration (30 min) and prolonged duration (120 min) in an attempt to restore distal acidification to normal. In posthypocapnic rats, hypercapnia of brief duration was associated with a significant increase in urine PCO2 and a fall in urine pH. Prolonged hypercapnia resulted in a marked increase in urine PCO2 and a further fall in urine pH. At any urinary bicarbonate concentration, however, the urine PCO2 and U-B PCO2 posthypocapnic rats exposed to hypercapnia were still significantly lower than in normal control rats identically subjected to prolonged hypercapnia and with comparable blood PCO2 and blood pH. Our findings indicate that distal acidification after abrupt recovery from chronic hypocapnia is decreased as if the kidneys were still under the influence of sustained hypocapnia. These findings could not be ascribed to extracellular alkalemia but could be explained by postulating that decreased urinary acidification resulted from persistence of cell alkalinity secondary to the accumulation of non-CO2 buffers generated during protracted hypocarbia. Alternatively, factors other than cell pH could mediate the adaptive decrease in distal hydrogen ion secretion of posthypocapnic rats.

Importance of medullary events in ammonium excretion: studies in acute respiratory and acute metabolic acidosis

1983 ◽  
Vol 61 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Andre Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
Marc Goldstein ◽  
Bobby Stinebaugh ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Respiratory Acidosis ◽  
Renal Medulla ◽  
Hydrogen Ion ◽  
Ammonium Excretion ◽  
Urine Ph ◽  
Ion Secretion ◽  
Medullary Collecting Duct ◽  
Acute Metabolic Acidosis

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary [Formula: see text]. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, [Formula: see text], and the urine minus blood [Formula: see text] difference (U-B [Formula: see text]) were lower during acute hypercapnia. In these experiments, the urine [Formula: see text] was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B [Formula: see text] was 5 ± 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary [Formula: see text] can modify this relationship.

The Ventilatory Response in Diabetic Ketoacidosis

1974 ◽  
Vol 46 (4) ◽  
pp. 539-549 ◽  
Author(s):  
M. Fulop ◽  
N. Dreyer ◽  
H. Tannenbaum
Keyword(s):  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Ventilatory Response ◽  
Hydrogen Ion ◽  
Inverse Relation ◽  
Bicarbonate Concentration ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Blood Ph ◽  
Ion Activity

1. Previous studies of the ventilatory response to metabolic acidosis have usually considered only patients with arterial blood pH above 7·10. To define the response during more severe acidaemia, arterial CO2 tension and pH were measured in fifty-three episodes of diabetic ketoacidosis, including twenty-four with pH below 7·10, and ten with pH below 7·00. 2. The relation between arterial CO2 tension, and both blood pH and plasma bicarbonate concentration, in these cases with generally severe metabolic acidaemia (mean pH 7·12 ± SD 0·13), was very similar to the relations between those variables found by others in patients with less severe acidaemia, such as that due to renal failure. 3. As arterial blood hydrogen ion activity increased, arterial CO2 tension decreased inversely, reflecting well-sustained hyperventilation, even during profound acidaemia. 4. The inverse relation between arterial CO2 tension and hydrogen ion activity suggests that during metabolic acidosis, alveolar ventilation increases in direct proportion to the increased blood hydrogen ion activity.

Hydrogen ion secretion by the rat distal nephron: adaptation to chronic alkali and acid ingestion

1983 ◽  
Vol 245 (3) ◽  
pp. F349-F358
Author(s):  
C. Kornandakieti ◽  
R. Grekin ◽  
R. L. Tannen
Keyword(s):  
Ion Transport ◽  
Rat Kidney ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Ion Secretion ◽  
Titratable Acid ◽  
Chronic Ingestion ◽  
Hydrogen Ion Transport ◽  
Secretory Capacity

Isolated rat kidneys perfused at a low bicarbonate concentration were subjected to increased rates of buffer excretion, provided as creatinine, in order to examine the maximal hydrogen ion secretory capacity of the distal nephron. Preliminary experiments with kidneys from normal rats indicated that the quantity of hydrogen ion that titrated creatinine from urine pH to a pH of 6.0, designated TA-pH 6.0, provided an index of net hydrogen ion secretion by a functional segment of the distal nephron. With this technique the response of distal nephron hydrogen ion transport to ingestion of both acid and alkali loads was examined. Perfused kidneys from rats with chronic metabolic acidosis, produced by drinking 1.5% NH4Cl for 3-5 days, excreted urine with a lower pH and higher total titratable acid and TA-pH 6.0 than appropriate controls. Perfused kidneys from rats that ingested NaHCO3 for 7 days exhibited a higher urine pH and lower rates of total titratable acid and TA-pH 6.0 than controls. By contrast, kidneys from rats acutely tube-fed NaHCO3 3 h prior to study showed no change in urinary acidification parameters. Thus, chronic ingestion of an acid load stimulates, and chronic ingestion of an alkali load inhibits, the intrinsic hydrogen ion secretory capacity of the rat kidney at a distal nephron site. This intrinsic adaptation of the hydrogen ion transport mechanism is not secondary to changes in aldosterone because rats that ingested NaHCO3 chronically had higher plasma aldosterone levels than controls.

Characterization of distal hydrogen ion secretion in acute respiratory alkalosis

1978 ◽  
Vol 235 (3) ◽  
pp. F203-F208
Author(s):  
J. T. Sehy ◽  
M. K. Roseman ◽  
J. A. Arruda ◽  
N. A. Kurtzman
Keyword(s):  
Respiratory Alkalosis ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Alkaline Urine ◽  
Ion Secretion

The effect of acute respiratory alkalosis (ARA) on distal nephron H+ secretion was evaluated by measuring urine-to-blood (U-B) Pco2 in dogs with highly alkaline urine (urine pH greater than 7.8). ARA led to a significant decrease in U-B Pco2 and in urine HCO3 concentration; urine pH, however, increased significantly, indicating that the decrease in urine Pco2 was of greater magnitude than the decrease in urine HCO3 concentration. For any given urine HCO3 concentration urine Pco2 was lower (i.e., urine pH was higher) in ARA than in controls. Administration of tris(hydroxymethyl)aminomethane (Tris) during ARA resulted in a significant increase in U-B Pco2 to control values. In animals with moderately alkaline urine (urine pH 6.4--7.4) and high urine PO4 concentration, ARA resulted in a significant decrease in UB-Pco2 and urine PO4 concentrations. Neutral PO4 infusion in these dogs resulted in an increase in urine PO4 concentration and U-B Pco2 to control levels. These data demonstrate that ARA results in a significant decrease in U-B Pco2 that is not solely attributable to changes in urine HCO3 concentration. The observation that Tris and PO4 infusion during ARA raises U-B Pco2 to control levels suggests that the ability to secrete H+ is intact.

scholarly journals Effect of blood pH on distal nephron hydrogen ion secretion

1980 ◽  
Vol 17 (5) ◽  
pp. 615-621 ◽  
Author(s):  
Andre Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
M.A. Robert Richardson ◽  
Siu-Cheung Tam ◽  
...  
Keyword(s):  
Hydrogen Ion ◽  
Distal Nephron ◽  
Ion Secretion ◽  
Blood Ph

scholarly journals On the mechanism of impaired distal acidification in hyperkalemic renal tubular acidosis: evaluation with amiloride and bumetanide.

1992 ◽  
Vol 3 (4) ◽  
pp. 953-964
Author(s):  
W Schlueter ◽  
T Keilani ◽  
M Hizon ◽  
B Kaplan ◽  
D C Batlle
Keyword(s):  
Single Dose ◽  
Renal Tubular Acidosis ◽  
Hydrogen Ion ◽  
Potassium Excretion ◽  
Urine Ph ◽  
Ion Secretion ◽  
Group I ◽  
Voltage Dependent ◽  
Group Ii ◽  
Renal Tubular

It has been postulated that a distinctive type of hyperkalemic distal renal tubular acidosis (DRTA), referred to as voltage-dependent DRTA, results from diminished potassium and hydrogen ion secretion in the distal nephron, which is due to a suboptimal voltage (lumen negative) as a result of impaired sodium reabsorption. To test for the presence of a voltage-dependent DRTA, we used amiloride (20 mg oral, single dose) and bumetanide (2 mg oral, single dose) to inhibit and to stimulate voltage-dependent potassium and hydrogen ion secretion, respectively. Eighteen patients with hyperkalemic DRTA and seven controls with a comparable degree of renal impairment were studied. Patients were subdivided in two groups on the basis of their ability to lower their urine pH during spontaneous acidosis. Patients in Group I lowered their urine pH to the level of controls (5.29 +/- 0.06 and 5.37 +/- 0.11, respectively) whereas patients in Group II could not lower their urine pH below 5.5 (6.38 +/- 0.11). Patients in Group I and Group II had a similar degree of metabolic acidosis and hyperkalemia whereas controls had neither acidosis or hyperkalemia. Most patients in Group II and all patients in Group I had low plasma aldosterone levels. The administration of amiloride resulted in an increase in urine pH and a decrease in potassium excretion in all three groups. The finding that amiloride, presumably by obliterating the transtubular voltage as a result of blockade of sodium transport, inhibited potassium excretion to about the same extent in both groups of patients and in controls argues against the existence of a voltage-dependent defect. Bumetanide produced a fall in urine pH below 5.5 and an increase in potassium excretion in controls and Group I patients. In Group II patients, bumetanide failed to elicit a fall in urine pH below 5.5 but resulted in an increase in potassium excretion similar to that seen in controls and Group I patients. These findings suggest that a derangement other than a voltage-dependent defect is responsible for the inability, characteristic of Group II patients, to lower their urine pH. It was concluded that the impairment in urinary acidification observed in patients with this subtype of hyperkalemic DRTA is due to a defect in collecting tubule hydrogen secretion that results from H+ ATPase dysfunction rather than from a voltage-dependent defect.

Time Course of Blood Bicarbonate and pH Three Hours After Sodium Bicarbonate Ingestion

2008 ◽  
Vol 3 (2) ◽  
pp. 240-242 ◽  
Author(s):  
Michael J. Price ◽  
Malkit Singh
Keyword(s):  
Sodium Bicarbonate ◽  
Time Course ◽  
Sodium Bicarbonate Solution ◽  
Bicarbonate Concentration ◽  
Blood Ph ◽  
Peak Blood

This study examined the increase in blood pH and bicarbonate concentration after ingestion of a standard sodium bicarbonate solution. Peak blood pH and bicarbonate concentration occurred between 60 and 90 minutes. Values decreased over the remainder of the ingestion period although still elevated above preingestion levels.

Renal electrolyte handling, acid-base status, and urinary acidification in Bufo marinus

1982 ◽  
Vol 243 (1) ◽  
pp. F60-F66
Author(s):  
S. Long
Keyword(s):  
Excretion Rate ◽  
Nonlinear Function ◽  
Acid Excretion ◽  
Urine Ph ◽  
Urinary Ph ◽  
Blood Ph ◽  
Urinary Acidification ◽  
Acid Base Status ◽  
Renal Responses ◽  
Secretion Rates

In hydrated toads reabsorption of 92% of filtered bicarbonate produces a urine of pH at 22 degrees C. Average blood-to-urine pH gradient is 0.8-0.9 U under these conditions but may reach 3-4 U. Net acid excretion rate in hydrated animals is approximately 30 mu eq . h-1 . kg-1. Flow-independent acid excretion is a negative nonlinear function of urinary pH and passes from positive to negative values in the range of normal urinary pH due to rapid rise in [HCO3-] and slower decline in [NH4+]. [H2PO4-] accounts for only 10-20% of buffer-bound acid excreted. Sulfate loading in Cl-restricted toads is without effect on blood pH but produces significant reduction in blood [Cl-]/[Na+] and in urinary pH, and increased urinary [K+] and net acid secretion rates relative to controls. These renal responses are diminished or absent during sulfate loading in Cl-rich toads. In both groups [Cl-] shows significant positive correlation with pH in sulfate-containing urines. These results are discussed in the context of the nonhomeostatic model of urinary acidification developed in mammals.

Reliability and Effect of Sodium Bicarbonate: Buffering and 2000-m Rowing Performance

2012 ◽  
Vol 7 (2) ◽  
pp. 152-160 ◽  
Author(s):  
Amelia J. Carr ◽  
Gary J. Slater ◽  
Christopher J. Gore ◽  
Brian Dawson ◽  
Louise M. Burke
Keyword(s):  
Calcium Carbonate ◽  
Confidence Interval ◽  
Sodium Bicarbonate ◽  
Pairwise Comparisons ◽  
Bicarbonate Concentration ◽  
Mean Power ◽  
Typical Error ◽  
Rowing Performance ◽  
Rowing Ergometer ◽  
Double Blinded

Purpose:The aim of this study was to determine the effect and reliability of acute and chronic sodium bicarbonate ingestion for 2000-m rowing ergometer performance (watts) and blood bicarbonate concentration [HCO3−].Methods:In a crossover study, 7 well-trained rowers performed paired 2000-m rowing ergometer trials under 3 double-blinded conditions: (1) 0.3 grams per kilogram of body mass (g/kg BM) acute bicarbonate; (2) 0.5 g/kg BM daily chronic bicarbonate for 3 d; and (3) calcium carbonate placebo, in semi-counterbalanced order. For 2000-m performance and [HCO3−], we examined differences in effects between conditions via pairwise comparisons, with differences interpreted in relation to the likelihood of exceeding smallest worthwhile change thresholds for each variable. We also calculated the within-subject variation (percent typical error).Results:There were only trivial differences in 2000-m performance between placebo (277 ± 60 W), acute bicarbonate (280 ± 65 W) and chronic bicarbonate (282 ± 65 W); however, [HCO3−] was substantially greater after acute bicarbonate, than with chronic loading and placebo. Typical error for 2000-m mean power was 2.1% (90% confidence interval 1.4 to 4.0%) for acute bicarbonate, 3.6% (2.5 to 7.0%) for chronic bicarbonate, and 1.6% (1.1 to 3.0%) for placebo. Postsupplementation [HCO3−] typical error was 7.3% (5.0 to 14.5%) for acute bicarbonate, 2.9% (2.0 to 5.7%) for chronic bicarbonate and 6.0% (1.4 to 11.9%) for placebo.Conclusion:Performance in 2000-m rowing ergometer trials may not substantially improve after acute or chronic bicarbonate loading. However, performances will be reliable with both acute and chronic bicarbonate loading protocols.

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