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.

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.

Adaptive changes in renal acidification in response to chronic respiratory acidosis

1985 ◽  
Vol 248 (4) ◽  
pp. F492-F499 ◽  
Author(s):  
R. L. Tannen ◽  
B. Hamid
Keyword(s):  
Metabolic Acidosis ◽  
Proton Transport ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Chronic Metabolic Acidosis ◽  
Adaptive Changes ◽  
Secretory Capacity

To examine whether chronic respiratory acidosis results in adaptive changes in renal acidification, rats were housed for 3 days in an environmental chamber with an ambient CO2 content of 10% and their kidneys were perfused in vitro according to two protocols. To assess hydrogen ion secretory capacity of the distal nephron, perfusions were carried out with a low bicarbonate concentration, in the absence of ammoniagenic substrate, and with saturating quantities of the buffer creatinine. Under these conditions, the titration of creatinine at a pH less than 6.0 (TA pH 6.0) reflects the H+ secretory capacity of a discrete functional segment of the distal nephron. Kidneys from rats with chronic respiratory acidosis exhibited a significantly lower urine pH and higher rate of TA pH 6.0 than controls perfused in this fashion, indicative of an adaptive increase in the distal nephron capacity for proton transport. This adaptation was comparable with that reported previously for rats exposed to chronic metabolic acidosis. Furthermore, evidence of adaptation persisted in the presence of amiloride (10(-5) M), suggesting that it reflects, at least in part, a sodium-independent mechanism of proton transport. Hydrogen ion secretion by the proximal nephron was assessed by performing standard bicarbonate titration curves with kidneys from rats with chronic respiratory acidosis, chronic metabolic acidosis, and controls using a perfusate equilibrated with 95% O2/5% CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

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 renal response of sheep to feeding

1964 ◽  
Vol 15 (2) ◽  
pp. 289 ◽  
Author(s):  
BD Stacy ◽  
AH Brook
Keyword(s):  
Renal Excretion ◽  
Extracellular Fluid ◽  
Urine Flow ◽  
Hydrogen Ion ◽  
Urine Ph ◽  
Renal Response ◽  
Alkaline Urine ◽  
Renal Clearances ◽  
Acute Changes ◽  
Sodium And Potassium

Acute changes in renal excretion occurred when pen-fed sheep were given their daily feed. There was a reduction in the rate of urine flow and the concentration of the urine increased. During the oliguric phase, sodium and potassium excretion decreased whereas hydrogen ion excretion increased and caused acidification (pH 5–6) of the normally alkaline urine (pH 7–8). Renal clearances of inulin and PAH did not indicate that the urinary changes were due to altered renal haemodynamics. It is suggested that the observed renal response was a reflection of the sudden shift of extracellular fluid into the gut at the onset of feeding.

Lack of Dependence of Urine Pco2 upon Reduction of Glomerular Filtration Rate in Alkalotic Dogs

1977 ◽  
Vol 52 (2) ◽  
pp. 119-123
Author(s):  
B. J. Stinebaugh ◽  
T. H. Hostetter ◽  
R. A. Peraino ◽  
F. X. Schloeder ◽  
W. N. Suki
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Flow ◽  
Hydrogen Ion ◽  
Alkaline Urine ◽  
Ion Secretion ◽  
Arterial Blood ◽  
Excretion Rates ◽  
Acute Changes

1. The Pco2 gradient between alkaline urine and arterial blood (U—B Pco2) is thought to depend primarily on distal hydrogen ion secretion. However, other variables affecting the U—B Pco2 include the urine flow rate, the urinary bicarbonate and phosphate excretion rates and the glomerular filtration rate. 2. In order to evaluate the effects of acute changes in these factors on the U—B Pco2, bicarbonate-loaded dogs with maximal U—B Pco2 values were subjected to either acute unilateral elevations of ureteral pressure or hypotension caused by nitroprusside infusion. The results demonstrate that acute reduction in the glomerular fiitration rate does not cause a decrease in the U—B Pco2 as long as the urinary concentrations of phosphate and bicarbonate do not decline. 3. Urinary concentrations of phosphate and bicarbonate appeared more important than their excretion rates in the maintenance of elevated U—B Pco2 values.

scholarly journals The effect of hyperventilation on distal nephron hydrogen ion secretion.

1976 ◽  
Vol 58 (1) ◽  
pp. 77-82 ◽  
Author(s):  
R A Giammarco ◽  
M B Goldstein ◽  
M L Halperin ◽  
B J Stinebaugh
Keyword(s):  
Hydrogen Ion ◽  
Distal Nephron ◽  
Ion Secretion

Effect of parathyroid hormone on urinary acidification

1977 ◽  
Vol 232 (5) ◽  
pp. F429-F433 ◽  
Author(s):  
J. A. Arruda ◽  
L. Nascimento ◽  
C. Westenfelder ◽  
N. A. Kurtzman
Keyword(s):  
Parathyroid Hormone ◽  
Renal Tubular Acidosis ◽  
Ammonium Excretion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Alkaline Urine ◽  
Acid Urine ◽  
Urinary Acidification ◽  
Before And After ◽  
Renal Tubular

The effect of parathyroid hormone (PTH) administration on urinary acidification was studied in intact and thyroparathyroidectomized dogs. PTH administration resulted in a significant increase in urine pH and HCO3 excretion. In dogs with maximally acid urine caused by Na2SO4 infusion PTH administration also led to a significant increase in urine pH and to a decrease in ammonium excretion. To examine the effect of PTH on H+ secretion in the distal nephron we measured the urine-blood (U-B) PCO2 gradient in dogs with maximally alkaline urine (urine pH greater than 7.8) before and after PTH administration. After infusion of the hormone, HCO3 excretion increased significantly but the U-B PCO2 gradient remained unchanged. The effects of PTH infusion on urinary acidification in animals with distal renal tubular acidosis caused by LiCl administration were also studied. PTH administration to these dogs increased HCO3 excretion to the same level seen in normal dogs. These data suggest that PTH does not inhibit distal H+ secretion but increases HCO3 excretion by depressing proximal HCO3 reabsorption.

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.

scholarly journals Furosemide reduces BK-αβ4-mediated K+ secretion in mice on an alkaline high-K+ diet

2019 ◽  
Vol 316 (2) ◽  
pp. F341-F350 ◽  
Author(s):  
Bangchen Wang ◽  
Jun Wang-France ◽  
Huaqing Li ◽  
Steven C. Sansom
Keyword(s):  
Plasma Aldosterone ◽  
Elevated Plasma ◽  
Wild Type ◽  
Distal Nephron ◽  
Urine Ph ◽  
Alkaline Urine ◽  
High K ◽  
K Secretion ◽  
Cardioprotective Effects ◽  
Apical Localization

Special high-K diets have cardioprotective effects and are often warranted in conjunction with diuretics such as furosemide for treating hypertension. However, it is not understood how a high-K diet (HK) influences the actions of diuretics on renal K+ handling. Furosemide acidifies the urine by increasing acid secretion via the Na+-H+ exchanger 3 (NHE3) in TAL and vacuolar H+-ATPase (V-ATPase) in the distal nephron. We previously found that an alkaline urine is required for large conductance Ca2+-activated K+ (BK)-αβ4-mediated K+ secretion in mice on HK. We therefore hypothesized that furosemide could reduce BK-αβ4-mediated K+ secretion by acidifying the urine. Treating with furosemide (drinking water) for 11 days led to decreased urine pH in both wild-type (WT) and BK-β4-knockout mice (BK-β4-KO) with increased V-ATPase expression and elevated plasma aldosterone levels. However, furosemide decreased renal K+ clearance and elevated plasma [K+] in WT but not BK-β4-KO. Western blotting and immunofluorescence staining showed that furosemide treatment decreased cortical expression of BK-β4 and reduced apical localization of BK-α in connecting tubules. Addition of the carbonic anhydrase inhibitor, acetazolamide, to furosemide water restored urine pH along with renal K+ clearance and plasma [K+] to control levels. Acetazolamide plus furosemide also restored the cortical expression of BK-β4 and BK-α in connecting tubules. These results indicate that in mice adapted to HK, furosemide reduces BK-αβ4-mediated K+ secretion by acidifying the urine.

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