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 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

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.

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 Renal Tubular Acidosis in the Postpartum Period: A Case Report and Literature Review

2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Carlos E. Duran ◽  
Mayra Estacio ◽  
Fredy Lozano ◽  
Esteban Echeverri ◽  
Maria Juliana Riascos ◽  
...  
Keyword(s):  
Renal Tubular Acidosis ◽  
Hydrogen Ion ◽  
Ion Permeability ◽  
Distal Nephron ◽  
Laboratory Findings ◽  
Case Presentation ◽  
Ion Secretion ◽  
Luminal Membrane ◽  
Renal Tubular ◽  
The Impact

Case Presentation. Distal renal tubular acidosis (dRTA) is characterized by impaired hydrogen ion secretion in the distal nephron resulting either from decreased net activity of the proton pump or from increased luminal membrane hydrogen ion permeability. Typical complications of dRTA include severe hypokalemia, normal anion gap metabolic acidosis, nephrolithiasis, and nephrocalcinosis. The patient is a 25-year-old woman in immediate puerperium with hypokalemia leading to paralysis, and the laboratory findings in this patients were concerning for dRTA. It is rare to encounter this entity during pregnancy, and the impact of this pathology is unknown.

scholarly journals Ion Transport and the Development of Hydrogen Ion Secretion in the Stomach of the Metamorphosing Bullfrog Tadpole

1969 ◽  
Vol 54 (1) ◽  
pp. 76-95 ◽  
Author(s):  
John G. Forte ◽  
Liangchai Limlomwongse ◽  
Dinkar K. Kasbekar
Keyword(s):  
Ion Transport ◽  
Active Transport ◽  
Hydrogen Ion ◽  
Equilibrium Potential ◽  
Flux Analysis ◽  
Cell Interior ◽  
Ion Secretion ◽  
Hcl Secretion ◽  
Bullfrog Tadpole ◽  
Induced Changes

Isolated bullfrog tadpole stomachs secrete H+ by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. At this stage the PD shows characteristic responses identical to those of the adult. The appearance of HCl secretion correlates well with other studies showing the morphogenesis of oxyntic cells. Prior to the development of H+ secretion tadpole stomachs maintain a PD similar in polarity and magnitude to that of the adult; i.e., secretory (S) side negative with respect to the nutrient (N) side. The interdependence with aerobic metabolism appeared to increase progressively through metamorphosis; however, glycolytic inhibitors always abolished the PD. Isotopic flux analysis showed that the transepithelial movement of Na+ was consistent with passive diffusion, whereas an active transport of Cl- from N to S was clearly indicated. Variations in [Na+], [K+], and [Cl-] in the bathing solutions induced changes consistent with the following functional description of the pre-H+-secreting tadpole stomach. (a) The S side is relatively permeable to Cl-, but not to Na+ or K+. (b) An equilibrium potential for K+ and Cl- exists at the N interface. (c) Ouabain abolishes the selective K+ permeablity at the N interface and reduces the total PD. (d) Effects of Na+ replacement by choline in the N solution become manifest only below 10–20 mM. It is concluded that prior to development of H+ secretion, the tadpole gastric PD is generated by a Cl- pump from N to S and a Na+ pump operating from the cell interior toward the N side.

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)

Alveolar hypercapnia augments pulmonary C-fiber responses to chemical stimulants: role of hydrogen ion

2002 ◽  
Vol 93 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Qihai Gu ◽  
Lu-Yuan Lee
Keyword(s):  
Hydrogen Ion ◽  
Right Atrial ◽  
Mechanical Stimuli ◽  
Hydrogen Ions ◽  
Lung Inflation ◽  
C Fibers ◽  
Arterial Blood ◽  
Blood Ph ◽  
C Fiber

To determine whether the excitabilities of pulmonary C fibers to chemical and mechanical stimuli are altered by CO2-induced acidosis, single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering CO2-enriched gas mixture (15% CO2, balance air) via the respirator inlet for 30 s, which rapidly lowered the arterial blood pH from a baseline of 7.40 ± 0.01 to 7.17 ± 0.02. Alveolar HPC markedly increased the responses of these C-fiber afferents to several chemical stimulants. For example, the C-fiber response to right atrial injection of the same dose of capsaicin (0.25–1.0 μg/kg) was significantly increased from 3.07 ± 0.70 impulses/s at control to 8.48 ± 1.52 impulses/s during HPC ( n = 27; P < 0.05), and this enhanced response returned to control within ∼10 min after termination of HPC. Similarly, alveolar HPC also induced significant increases in the C-fiber responses to right atrial injections of phenylbiguanide (4–8 μg/kg) and adenosine (0.2 mg/kg). In contrast, HPC did not change the response of pulmonary C fibers to lung inflation. Furthermore, the peak response of these C fibers to capsaicin during HPC was greatly attenuated when the HPC-induced acidosis was buffered by infusion of bicarbonate (1.36–1.82 mmol · kg−1 · min−1 for 35 s). In conclusion, alveolar HPC augments the responses of these afferents to various chemical stimulants, and this potentiating effect of CO2 is mediated through the action of hydrogen ions on the C-fiber sensory terminals.

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