Renal Mechanisms for Excretion of Potassium

Berliner, Robert W.; Kennedy, Thomas J.; Hilton, James G.

doi:10.1152/ajplegacy.1950.162.2.348

Cited by 222 publications

(115 citation statements)

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“…This ratio in the case of sodium coincides almost exactly with mean values already reported in man and other animals (17)(18)(19)(20)(21)(22)(23). The distribution coefficient of potassium approximated that found in work on dogs (20) and in recent studies of Folk, Zierler, and Lilienthal (23) as well as of Berliner, Kennedy, and Hilton (24). Such distribution ratios of sodium and potassium confirm the assumption usually made with respect to concentrations of the ions in extracellular fluid in relation to certain balance calculations (4,25).…”

Section: Discussionsupporting

confidence: 89%

The Ultrafiltrability of Potassium and Sodium in Human Serum

Tarail¹,

Hacker²,

Taymor³

1952

J. Clin. Invest.

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One of the puzzling clinical aspects of the metabolism of electrolytes is the genesis of symptoms and signs of potassium depletion and potassium intoxication (1-3). Precipitous flaccid paralysis, sensory disturbances and respiratory failure, altogether analogous to the sequence of events in familial periodic paralysis, may occur in these disturbances of potassium metabolism characterized by either deficit or plethora of the ion. The preponderance of evidence indicates that such gross clinical derangements are observed in but a minority of instances of abnormality in the metabolism of potassium (1-9). Review of existing data, furthermore, fails to disclose a clinical, chemical, or physiologic difference which could account for the capricious incidence of serious manifestations in this minority of patients.The extensive metabolic studies of Jantz (10) in nine cases of familial periodic paralysis seem to afford a clue to the solution of this problem. He found that episodes of paralysis could be consistently related to a profound reduction in the ultrafiltrable fraction of plasma potassium. Although this finding has not been confirmed or negated, such an explanation might in part account for paralytic phenomena which occasionally supervene in patients without familial periodic paralysis, who develop disturbances of potassium metabolism.The present investigation comprises an analysis of the diffusibility in vitro of potassium and sodium of sera obtained from a group of normal subjects and an analogous preliminary survey of patients with derangements of electrolyte metabolism. The normal subjects were 24 medical students of the freshman class of Boston University School of Medicine. Patients in various states of electrolyte imbalance and dehydration were studied from the wards of Boston City Hospital. Normal subjects came to the laboratory following an overnight fast. Blood was withdrawn, using minimal stasis, under mineral oil, and serum was separated anaerobically within one hour of clot format A portion of serum from the centrifuged blood was aspirated from beneath its thin protective coat of oil into Lavietes' ultrafiltration chambers (11). Anaerobic ultrafiltration transpired through cellophane membranes at room temperature for about 48 hours. Technical details and equipment were identical with those described by Lavietes (11). Both original serum and ultrafiltrate were analyzed simultaneously. Serum residue was not analyzed.Sodium and potassium were determined on the Barclay flame photometer using lithium as the internal standard (12). All fluids were analyzed in duplicate-ie., two separate dilutions of 1 to 50 and 1 to 100 for potassium and 1 to 200 and 1 to 400 for sodium. Each unknown solution was "bracketed" by two knowns, and serum and corresponding ultrafiltrate were read together. Final values were averages of the results of two or more readings of each unknown solution. Average readings of duplicate dilutions were within 2% of one another. Before each group of determinations, the accuracy and precision o...

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Section: Discussionsupporting

confidence: 89%

The Ultrafiltrability of Potassium and Sodium in Human Serum

Tarail¹,

Hacker²,

Taymor³

1952

J. Clin. Invest.

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“…The protocol conformed to the NZH Guide fbr the Care and Use of' The potassium secretory response of the amiloride-sensitive ~~b~~~~~~~ ~~i~~l~ and was approved by the ,,aboratory segments of the immature n e~h r o n to acute potassium loading (10).…”

Section: Methodsmentioning

confidence: 99%

“…Dietary potassium supplementation enhances distal 29). Moreover, if chronic potassium supplementation of the n e~h r o n Dotassium secretion and urinam Dotassium excretion newborn dog increases Na,K-ATPase activity in potassium seunder baseline conditions (9, 2 1, 24-3 1) as &ell as during potassium loading (9,10,(27)(28)(29)(30)(31). This enhanced secretory capacity is at first the result of an increase in Na-K pump turnover rate without a change in pump number (23,28).…”

Section: Mean (Sem)mentioning

confidence: 99%

The Role of Cortical Na,K-ATPase in Distal Nephron Potassium Secretion by the Immature Canine Kidney

1991

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ABSTRACT. Amiloride-sensitive potassium secretion in response to acute potassium loading is lower in the newborn than in the adult. Potassium secretion is a function of late distal tubule and cortical collecting tubule Na,K-ATPase activity. Na,K-ATPase activity in vivo is determined by enzyme abundance and catalytic turnover. Chronic potassium supplementation increases potassium secretory capacity in the adult by increasing enzyme abundance in the late distal and cortical collecting tubules. We hypothesized that the lower potassium secretory capacity of the newborn was the result of lower late distal and cortical collecting tubule Na,K-ATPase activity and could be similarly enhanced. To test this hypothesis, newborn dogs were supplemented with 6 mmol KC1.d-'. kg-' for 1 wk; agematched litter mate controls were not ( n = 8 pairs). Potassium supplementation resulted in a mean increase in V,,, Na,K-ATPase activity in vitro (proportional to pump abundance) of 70 + 42%. Mean Na,K-ATPase activities + S E M were 279 + 58 versus 198 2 44 nmol inorganic P.h-I-gg DNA-', p = 0.05. However, amiloride-sensitive potassium secretion after an acute potassium load of 20 pmol. min-'. kg-' over 150 min was not enhanced (9.6 +-1.8 versus 8.9 + 0.8 pmol . min-' .kg-', potassium-supplemented versus control animals). We conclude that lower enzyme abundance is not primarily responsible for the newborn's lower potassium secretory capacity. W e speculate that the factor that limits secretion in the newborn during acute potassium loading does so by restricting catalytic turnover of the enzyme in vivo. (Pediatr Res 30: 457-463,1991) Abbreviations KIl2, substrate concentration at which the reaction velocity is half maximum Na,K-ATPase, sodium-potassium-activated adenosine triphosphatase T ' H~~, free water reabsorption TFK, tubular fluid potassium concentration TTKG, transtubular potassium gradient is less than that of the mature nephron (1). Transtubular potassium secretion in these nephron segments is driven by basolateral membrane Na,K-ATPase (2, 3). Na,K-ATPase activity has been shown to be lower in neonatal than adult nephron segments (4-6). It is possible, therefore, that the potassium secretory response of the immature nephron may be limited by lower Na,K-ATPase activity.Results of a study that examined the effect of increasing Na,KATPase activity on the renal response to acute potassium loading in newborn dogs did not support this possibility (7). In that study, newborn dogs were subjected to chronic potassium supplementation for 1 to 3 wk after birth to enhance Na,K-ATPase activity in potassium secretory nephron segment(s). Chronic potassium supplementation doubled V,,, cortical Na,K-ATPase activity compared with controls (who received distilled water supplementation), but did not enhance urinary excretion of an acute potassium load in the newborn dog. These results were interpreted to indicate that Na,K-ATPase pump abundance is not rate limiting in excretion of a potassium load in the newborn. However, it is possible that wate...

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“…It will be shown later that both processes may have a common mechanism. The renal secretion of potassium has previously been demonstrated during the intravenous infusion of potassium salts (Berliner, Kennedy & Hilton, 1950), in dehydration and in an osmotic diuresis (Mudge, Foulkes & Gilman, 1948). In the present dog experiments no extra potassium salts were given, and the ratio of the minute urine volume to the filtration rate (U V/CIN) did not exceed 0.1, the level at which an osmotic diuresis begins to provoke an increase in potassium excretion.…”

Section: Alkalosis and Potassium Excretionmentioning

confidence: 94%

“…During the infusion of sodium bicarbonate the dogs were in a positive sodium balance, and the filtered load of this ion was increased. Under these conditions part of the increment in potassium excretion may be attributed to an exchange of Na+ for K+ in the cells of the renal tubules, a mechanism which has been described by Berliner et al (1950). Indeed, a normal sodium balance may be essential for a high rate of potassium excretion during alkalosis.…”

Section: Alkalosis and Potassium Excretionmentioning

confidence: 97%