The renal response to acid loads in metabolic alkalosis; an assessment of the mechanisms regulating acid excretion.

Tannen, Richard L.; Bleich, Howard L.; Schwartz, William B.

doi:10.1172/jci105370

Cited by 33 publications

(26 citation statements)

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“…The possibility cannot be excluded, however, that the composition of renal tubular cells did not parallel that of the blood and body tissues generally, but rather that these cells became potassium deficient and acidotic. To account for the observed augmentation of acid excretion on this basis, we must also postulate that before the administration of potassium the potassium-depleted dogs had normal tubular potassium stores; as has been discussed previously, this seems unlikely (3).…”

Section: Discussionmentioning

confidence: 94%

“…For this purpose an experimental setting was chosen in which plasma bicarbonate concentration and pH were normal despite the presence of severe potassium deficiency, conditions conveniently provided by the dogs described in the previous paper (3) in which metabolic alkalosis was corrected by administration of hydrochloric acid and an electrolyte-free diet. The administration of potassium with a poorly reabsorbable anion has made it possible to determine whether, under these circumstances, the organism gives priority to conservation of sodium, to repair of potassium deficiency, or to maintenance of acid-base equilibrium.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies in both dog and man have challenged the widely held concept that repair of potassium deficiency is a prerequisite to the correction of metabolic alkalosis; ready and sustained correction of alkalosis has been shown to follow the administration of chloride, as either sodium chloride or hydrochloric acid, even when the diet is free of potassium (1)(2)(3)(4). Furthermore, it has been shown that correction of an alkalosis by hydrochloric acid is sometimes retarded by the simultaneous repair of potassium and sodium deficiency (3).…”

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confidence: 99%

“…Furthermore, it has been shown that correction of an alkalosis by hydrochloric acid is sometimes retarded by the simultaneous repair of potassium and sodium deficiency (3). In view of these observations an attempt has been made to explore further the relationship between the retention of potassium and the renal regulation of acid-base equilibrium.…”

mentioning

confidence: 99%

“…After drainage had been completed and a steady state of alkalosis achieved, the electrolyte supplement was withdrawn from the diet, and hydrochloric acid was administered until plasma bicarbonate and pH returned to control values. During the next 5 to 7 days, despite the presence of severe potassium depletion, a new steady state was reached in which the acid-base composition of extracellular fluid was normal and net acid excretion was virtually constant (3).…”

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confidence: 99%

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The induction of metabolic alkalosis by correction of potassium deficiency.

Bleich¹,

Tannen²,

Schwartz³

1966

J. Clin. Invest.

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Recent studies in both dog and man have challenged the widely held concept that repair of potassium deficiency is a prerequisite to the correction of metabolic alkalosis; ready and sustained correction of alkalosis has been shown to follow the administration of chloride, as either sodium chloride or hydrochloric acid, even when the diet is free of potassium (1-4). Furthermore, it has been shown that correction of an alkalosis by hydrochloric acid is sometimes retarded by the simultaneous repair of potassium and sodium deficiency (3). In view of these observations an attempt has been made to explore further the relationship between the retention of potassium and the renal regulation of acid-base equilibrium. For this purpose potassium-depleted animals with normal plasma bicarbonate concentrations were maintained on an electrolyte-free intake and then fed potassium with a poorly reabsorbable anion, either sulfate or phosphate. The data demonstrate that this experimental procedure induced a striking retention of potassium, a virtually equivalent increase in the renal excretion of acid, and a sustained metabolic alkalosis. MethodsBalance studies were carried out on six female mongrel dogs weighing between 18.3 and 26.3 kg. The dogs had been prepared according to the following protocol, which is described in greater detail in the previous paper (3): Animals were placed on an electrolyte-free diet supplemented daily with 40 mEq of sodium and 40 mEq of potassium as the neutral phosphate. Metabolic alkalosis, hypokalemia, and potassium deficiency were then in-

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The induction of metabolic alkalosis by correction of potassium deficiency.

Bleich¹,

Tannen²,

Schwartz³

1966

J. Clin. Invest.

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Renal Acidification: Integrated Tubular Responses

Cogan

Quan

1992

Comprehensive Physiology

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The sections in this article are: Normal Acidification by Nephron Segments Overview of Mechanisms of Acidification Rates of Acidification pH Gradient Physiological Roles of Normal Renal Acidification Renal Response to Change in Glomerular Filtration Rate and Luminal Flow Rate Bicarbonate Reabsorption Renal Response to Decrease in Plasma Bicarbonate Concentration: Metabolic Acidosis Bicarbonate Reabsorption Ammonium Formation Titratable Acid Formation Integrated Nephron Response: Renal Net Acid Excretion Renal Response to Increase in Plasma Bicarbonate Concentration: Metabolic Alkalosis Exogenous Bicarbonate Administration without Extracellular Volume Contraction or Potassium Depletion Bicarbonate Generation or Administration in the Setting of Chloride and Potassium Deficiencies Renal Response to Alterations in Plasma Bicarbonate Reabsorption Ammonium and Titratable Acid Formation Integrated Nephron Response: Bicarbonate Reabsorption and Net Acid Excretion by the Whole Kidney

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Renal acification during chronic hypercapnia in the conscious dog

Adrogué

Madias

1986

Pflugers Arch.

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Enhanced renal acidification during chronic hypercapnia (CH) results in transient augmentation in net acid excretion (NAE) (adaptation phase) and persistent acceleration in renal bicarbonate reclamation (adaptation and steady-state phases). The mechanisms responsible for the return of NAE to control values despite persistent acidemia during the steady state phase of CH remain undefined. In addition, it remains unsettled whether the enhancement of renal ammoniagenesis known to occur during the adaptation phase of CH persists during the steady-state phase. Furthermore it is uncertain if the alteration in whole-kidney acidification observed in CH originates from augmentation in the acidification of both proximal and distal nephronal segments. To shed further light on these issues, observations on the profile of the urine acid-base moieties during the adaptive and steady-state phases of CH were carried out in dogs chronically exposed to hypercapnia (10% FiCO2) in an environmental chamber (13 days). Additionally, collecting duct hydrogen ion secretion (CDH+S) was evaluated by employing the U-B PCO2 in alkaline urine in intact unanesthetized dogs with either CH (10% FiCO2) or eucapnia. The balance studies demonstrated that NAE increased in early hypercapnia (4.84 meq/kg body weight, control 3.27 meq/kg body weight, p less than 0.05) and returned to baseline thereafter; by contrast, urine NH+4 which was augmented during the adaptation phase (3.71 meq/kg body weight, control 1.97 meq/kg body weight, p less than 0.05) remained elevated throughout (3.25 meq/kg body weight).(ABSTRACT TRUNCATED AT 250 WORDS)

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The renal response to acid loads in metabolic alkalosis; an assessment of the mechanisms regulating acid excretion.

Cited by 33 publications

References 16 publications

The induction of metabolic alkalosis by correction of potassium deficiency.

The induction of metabolic alkalosis by correction of potassium deficiency.

Renal Acidification: Integrated Tubular Responses

Renal acification during chronic hypercapnia in the conscious dog

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