The Extrarenal Correction of Alkalosis Associated With Potassium Deficiency 1

Cooke, Robert E.; Segar, William E.; Cheek, Donald B.; Coville, Frances; Darrow, Daniel C.

doi:10.1172/jci102665

Cited by 203 publications

(49 citation statements)

References 8 publications

(7 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since serum potassium concentration did not decline, nitrogen balance did not change significantly, and organic acid excretion increased only slightly, the increment in potassium excretion must chiefly represent intracellular cation exchanged for hydrogen ion. Cellular uptake of hydrogen in exchange for potassium occurs when tissue is depleted of potassium by administration of DOCA and low potassium diets (13,14), and the present observations demonstrate that a similar exchange may occur in reverse sequence, as a result of primary cellular penetration of hydrogen. In two of the preshydrogen buffering might occur.…”

Section: B Post-acidification Periodsupporting

confidence: 60%

The Disposition of Acid Administered to Sodium-Depleted Subjects: The Renal Response and the Role of the Whole Body Buffers 12

Schwartz¹,

Jenson²,

Relman³

1954

J. Clin. Invest.

View full text Add to dashboard Cite

Previous studies (1-4) on the response of normal human subjects to the administration of mineral acids or acidifying salts have established that: 1) Extracellular bicarbonate concentration and pH are reduced; and 2) there is a prompt increase in the renal excretion of the administered anion accompanied at first mainly by sodium, potassium, and small amounts of ammonium. Ammonium excretion rises slowly, and after a few days replaces most of the fixed cation in the urine.Little is known about the mechanisms regulating this renal response, or how it might be modified. Furthermore, although it is evident that the moiety of administered hydrogen not immediately appearing in the urine as ammonium or titratable acid must be accounted for by changes in body buffers, no description has been made of the internal distribution of the retained hydrogen ions. It was pointed out many years ago (5, 6) that buffers other than those in whole blood must be important in this process, but there are no quantitative data on the relative importance of red cell, plasma, interstitial fluid, and cellular buffers.In the present study, acidifying salts were administered to healthy subjects who had previously been depleted of sodium. The purposes of this investigation were : 1) To attempt a quantitative description of the internal distribution of the retained hydrogen ion and thereby clarify the relative importance of the various body buffers in the extrarenal adjustments to acid loading; and 2) to 1 This study was supported in part by grants from the National Heart Institute of the National Institutes of Health, U.S.P.H.S., the Greater Boston Chapter of the Massachusetts Heart Association and from the Research and Development Bcard, Surgeon General's Office, Department of the Army.2 Presented in abstract at the 45th annual meeting of the American Society for Clinical Investigation, May, 1953. determine how sodium depletion might modify the nature of the cation diuresis, and particularly how it might change the renal ammonium response. METHODSFive balance studies were carried out on five healthy male medical students. Sodium depletion was produced over a period of four to five days by a low-sodium diet (10 to 20 mEq. per day) and a total of one to three inj ections of a mercurial diuretic. During this period the subjects lost an average of 2.4 Kg. (range: 1.7 to 2.7 Kg.). The low-sodium diet was continued and the balance study was begun with a control period of at least four days, during which time serum concentrations and urinary excretion of electrolytes were approximately constant. Following this, three subjects were given ammonium chloride (721 to 1028 mEq. of chloride) and two subjects ammonium sulfate (400 and 504 mEq. of sulfate) in divided oral doses over a two to three-day period. In each instance a post-treatment period of one or more days was obtained. The subjects were allowed to continue their usual activities during the period of study but were instructed to avoid exertion.Urine inorganic sulfate was determined gravimetrical...

show abstract

Section: B Post-acidification Periodsupporting

confidence: 60%

The Disposition of Acid Administered to Sodium-Depleted Subjects: The Renal Response and the Role of the Whole Body Buffers 12

Schwartz¹,

Jenson²,

Relman³

1954

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…It has been suggested that the alkalosis usually present in potassium deficiency may be due, at least in part, to exchange of intracellular potassiumi for extracellular hydrogen ions (31,32). The approximate equivalence of the sodium and potassium shifts listed in Figures 5 and 6 show that, contrary to prevailing hypotheses (33), changes in aimimonium excretion were independent of changes in urine pH.…”

Section: Discussionmentioning

confidence: 77%

Metabolic and Renal Studies in Chronic Potassium Depletion Resulting From Overuse of Laxatives 12

Schwartz¹,

Relman²

1953

J. Clin. Invest.

239

View full text Add to dashboard Cite

“…In a study of experimental potassium deficiency just published by Cooke and colleagues (23) it was also concluded that there is a transport of hydrogen into the cell in the alkalosis of potassium deficiency.…”

Section: Addendummentioning

confidence: 99%

Effect of Potassium Deficiency on Carbon Dioxide, Cation, and Phosphate Content of Muscle

Gardner

MacLachlan

Berman

1952

Journal of General Physiology

View full text Add to dashboard Cite

Albino rats weighing 160 to 175 gm. were fed a complete synthetic diet containing 0.003 per cent potassium and 0.7 per cent sodium for 40 days. Controls were given the same diet plus adequate added potassium. 1. Data from analyses of serum and skeletal muscle showed (a) a fall in serum chloride concentration and an increase in serum carbon dioxide concentration and pH in the potassium-deficient rats; (b) increases of sodium, magnesium, and calcium and a decrease of potassium in the muscle of the potassium-deficient rats; (c) no change of muscle chloride or carbon dioxide concentrations in the potassium-deficient rats. (2) Application of the Wallace-Hastings calculations to these data revealed (a) intracellular pH of the skeletal muscle of the normal rat to be 6.98 ± 0.08; (b) an increase in serum partial pressure of carbon dioxide (pCO2) in potassium deficiency, together with increases in concentrations of [H2CO2] and [HCO3-] per kg. extracellular water and [H2CO3] per kg. cell water; (c) a decrease in values for [CO2] and [HCO3-] per kg. intracellular water; (d) a fall of intracellular pH in potassium deficiency to 6.42 ± 0.05. (3) Analyses of sacrospinalis muscle from five men undergoing operation for ruptured intervertebral disc showed a mean value of 9.46 ± 1.31 mM carbon dioxide per kg. blood-free tissue. Some problems of interpretation of data are briefly discussed.

show abstract

The Extrarenal Correction of Alkalosis Associated With Potassium Deficiency 1

Cited by 203 publications

References 8 publications

The Disposition of Acid Administered to Sodium-Depleted Subjects: The Renal Response and the Role of the Whole Body Buffers 12

The Disposition of Acid Administered to Sodium-Depleted Subjects: The Renal Response and the Role of the Whole Body Buffers 12

Metabolic and Renal Studies in Chronic Potassium Depletion Resulting From Overuse of Laxatives 12

Effect of Potassium Deficiency on Carbon Dioxide, Cation, and Phosphate Content of Muscle

Contact Info

Product

Resources

About