Effect of insulin on renal potassium metabolism

1987 ◽  
Vol 252 (1) ◽  
pp. F60-F64 ◽  
Author(s):  
L. Rossetti ◽  
G. Klein-Robbenhaar ◽  
G. Giebisch ◽  
D. Smith ◽  
R. DeFronzo
Keyword(s):  
Potassium Concentration ◽  
Insulin Dose ◽  
Plasma Potassium ◽  
High Dose ◽  
Base Line ◽  
Potassium Excretion ◽  
Insulin Clamp ◽  
Urinary Potassium ◽  
Plasma Insulin Levels ◽  
Renal Potassium Excretion

The effect of insulin on renal potassium excretion was examined by employing the euglycemic insulin clamp technique in combination with renal clearance measurements. While euglycemia was maintained, insulin was infused at rates of 4.8 (n = 7) and 12 (n = 5) mU X kg-1 X min-1. Steady-state plasma insulin levels of 164 +/- 8 and 370 +/- 15 microU/ml were achieved in the low- and high-dose studies, respectively. Base-line plasma potassium concentration declined progressively by a mean of 0.14 +/- 0.09 (P less than 0.05) and 0.40 +/- 0.05 meq/liter (P less than 0.01) during the low- and high-dose insulin infusion protocols. Urinary potassium excretion did not change significantly from base line with either insulin dose. Because the decline in plasma potassium concentration could have masked a stimulatory effect of insulin on UKV, six rats received a 12-mU X kg-1 X min-1 euglycemic insulin clamp in combination with an exogenous potassium infusion to maintain the plasma potassium concentration constant at the basal level (4.03 +/- 0.03 vs. 4.05 +/- 0.05 meq/l). Under these conditions of normokalemia, insulin augmented UKV 2.4-fold, from 0.20 +/- 0.05 to 0.48 +/- 0.04 meq/l (P less than 0.001).

Interrelated effects of aldosterone and plasma potassium on potassium excretion

1983 ◽  
Vol 244 (1) ◽  
pp. F28-F34 ◽  
Author(s):  
D. B. Young ◽  
A. W. Paulsen
Keyword(s):  
Renal Function ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Normal Range ◽  
Potassium Intake ◽  
Group I ◽  
Urinary Potassium ◽  
The Relationship ◽  
Renal Potassium Excretion

The interacting effects of aldosterone and plasma potassium concentration on steady-state renal potassium excretion were studied in two groups of chronically adrenalectomized dogs. In group I (six dogs, 22.9 kg) aldosterone was infused intravenously at 20 micrograms/day while potassium intake was changed in steps of 7-10 days duration from 10 to 30 to 100 meq/day. At the completion of each step, plasma potassium concentration, urinary potassium excretion, and other variables that potentially may affect renal function were measured. In group II (six dogs, 22.2 kg) a similar protocol was followed except that aldosterone was infused at 250 micrograms/day and the potassium intake levels were 30, 100, and 200 meq/day. Plasma potassium concentration and excretion data for the 20 micrograms/day group were: 3.22 +/- 0.26 meq/liter and 5 +/- 1 meq/day, 4.35 +/- 0.08 meq/liter and 21 +/- 2 meq/day, and 5.88 meq/liter and 82 +/- 3 meq/day at the 10, 30, and 100 meq/day intake levels, respectively. For the 250 micrograms/day group the values were: 2.72 +/- 0.18 meq/liter and 28 +/- 7 meq/day, 4.16 +/- 0.14 meq/liter and 71 +/- 8 meq/day, and 4.40 +/- 0.14 meq/liter and 172 +/- 26 meq/day at the 30, 100, and 200 meq/day intake levels. Therefore, the increase in aldosterone infusion rate shifted the relationship between plasma potassium concentration and potassium excretion to the left so that at a given level of plasma potassium a greater amount of potassium was excreted. In the normal range of plasma potassium concentration (4.00-4.40 meq/liter) the increase in aldosterone levels resulted in a four- to eightfold increase in daily potassium excretion.

Circadian variation of intercompartmental potassium fluxes in man

1975 ◽  
Vol 38 (1) ◽  
pp. 163-170 ◽  
Author(s):  
M. C. Moore Ede ◽  
M. F. Brennan ◽  
M. R. Ball
Keyword(s):  
Dietary Intake ◽  
Potassium Concentration ◽  
Circadian Variation ◽  
Plasma Potassium ◽  
Diurnal Variations ◽  
Potassium Content ◽  
Extracellular Potassium ◽  
Potassium Excretion ◽  
Urinary Potassium ◽  
Net Flux

Circadian rhythms of plasma potassium concentration and urinary potassium excretion persisted in three normal volunteers when diurnal variations in activity, posture, and dietary intake were eliminated for 3–10 days. Measurements of the arteriovenous difference in plasma potassium concentration across the resting forearm and of erythrocyte potassium concentration suggested that there is a net flux of potassium from ICF to ECF in the early morning and a reverse net flux later in the day. The total net ICF-ECF fluxes were estimated from the diurnal variations in extracellular potassium content corrected for dietary intake and urinary potassium loss. The net fluxes between ICF and ECF were found to be counterbalanced by the circadian rhythm in urinary potassium excretion. Desynchronization of these rhythms would result in marked fluctuations in extracellular potassium content. These findings suggest that some revision is required of the concept of basal state in potassium homeostasis.

Relationship between plasma potassium concentration and renal potassium excretion

1982 ◽  
Vol 242 (6) ◽  
pp. F599-F603 ◽  
Author(s):  
D. B. Young
Keyword(s):  
Renal Excretion ◽  
Potassium Concentration ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Potassium Intake ◽  
Arterial Ph ◽  
The Relationship ◽  
Renal Potassium Excretion

To study the relationship between extracellular potassium concentration and renal excretion of potassium, seven chronically adrenalectomized dogs were maintained on a constant intravenous infusion of aldosterone (50 micrograms/day), and constant sodium intake (30 meq/day ) while they received four levels of potassium intake--10, 30, 100, and 200 meq/day--for 7-10 days each. At the conclusion of each level of intake, plasma potassium and renal excretion as well as other variables known to influence potassium excretion were measured. There were minimal changes in arterial pH, mean arterial pressure, extracellular fluid volume, or glomerular filtration rate at any level of potassium intake. The values for plasma potassium and renal potassium excretion attained at each level of intake were: 3.13 +/- 0.24 and 10 +/- 2; 4.18 +/- 0.18 and 21 +/- 6; 4.31 +/- 0.11 and 66 +/- 10; and 4.75 +/- 0.10 meq/liter and 170 +/- 16 meq/day, respectively. Under these experimental conditions in which the levels of aldosterone, sodium intake, arterial pH, arterial pressure, extracellular fluid volume, and glomerular filtration rate remain constant, plasma potassium concentration appears to have a week effect on renal potassium excretion below the normal level of plasma potassium (approx. 11 meq/day change in excretion for each milliequivalent per liter change in concentration). Above the normal level, however, plasma potassium concentration has a powerful effect, 260 meq/day per milliequivalent per liter. The characteristics of the relationship between plasma potassium and renal potassium excretion make it ideally suited for controlling potassium excretion in response to greater than normal potassium intake.

Acute hypokalemic effect of gossypol

1986 ◽  
Vol 64 (7) ◽  
pp. 881-884 ◽  
Author(s):  
Siu-Cheung Tam
Keyword(s):  
Clinical Trials ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Minimal Change ◽  
Potassium Excretion ◽  
Fluid Compartment ◽  
Urinary Potassium ◽  
Chronic Ingestion

Clinical trials had demonstrated that chronic ingestion of gossypol induced infertility in males. Hypokalemia of various severities were reported in volunteers taking gossypol. The purpose of this study is to investigate the effects of acute gossypol infusion into alkalotic rats. Plasma potassium concentration decreased from 4.08 to 2.87 mM after gossypol infusion with minimal change in urinary potassium excretion. The hypokalemic effect of gossypol was also observed in nephretomized rats. Some of the factors that are known to affect potassium distribution between the extracellular and intracellular fluid compartment have been investigated in these rats. Plasma glucose concentration was not significantly altered. Gossypol induced hypokalemia was not blocked in rats treated with propranolol. It is therefore believed that the acute hypokalemic effect of gossypol is a direct shifting of potassium into cells.

Urinary Potassium Excretion in the Critically III Neonate

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 259-264
Author(s):  
William D. Engle ◽  
Billy S. Arant
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Plasma Potassium ◽  
Preterm Neonates ◽  
Prostaglandin E ◽  
Potassium Excretion ◽  
Potassium Balance ◽  
Frequent Use ◽  
Urinary Potassium

The possibility that negative potassium balance may occur in critically ill preterm neonates is suggested by factors such as the usual provision of minimal potassium intake, increased plasma aldosterone concentrations, increased prostaglandin synthesis, and the frequent use of diuretic agents. In order to assess the relationship between potassium balance and renal prostaglandins, nine infants with respiratory distress syndrome (mean birth weight 1,264 g, mean gestational age 30.6 weeks) were studied sequentially with timed-urine collections during the first four postnatal days and values were compared with those of 18 preterm infants without respiratory distress syndrome. Mean plasma potassium concentrations decreased significantly from 4.87 ± 0.19 mEq/L (mean ± SEM) on day 1 to 3.83 ± 0.18 mEq/L on day 4, (P < 0.05), and cumulative potassium balance was -4.07 ± 0.95 mEq/kg or 10% of estimated total body potassium. Urinary excretion of prostaglandin E, on day 1 in infants with respiratory distress syndrome was significantly greater than in those without respiratory distress syndrome (22.0 ± 4.9 v 8.3 ± 1.6 ng/mg of creatinine) and varied directly with urinary potassium excretion (r = .66, P < .001). These studies suggest that consideration be given to the importance of providing sufficient potassium to prevent hypokalemia in the stressed preterm infant and that pharmacologic agents that alter prostaglandins or potassium excretion should be used with caution.

Effects of sodium intake on steady-state potassium excretion

1984 ◽  
Vol 246 (6) ◽  
pp. F772-F778 ◽  
Author(s):  
D. B. Young ◽  
T. E. Jackson ◽  
U. Tipayamontri ◽  
R. C. Scott
Keyword(s):  
Steady State ◽  
Potassium Concentration ◽  
Sodium Intake ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Concentration Data ◽  
Potassium Intake ◽  
Independent Variable ◽  
The Relationship

The effects of changes in sodium intake on the steady-state relationship between plasma potassium concentration and potassium excretion were studied in 15 chronically adrenalectomized dogs. Throughout the experiments the dogs received aldosterone at a rate of 50 micrograms/day and methylprednisolone at 1 mg/day. The relationship between plasma potassium and steady-state potassium excretion was obtained by changing potassium intake from 10 to 30 to 100 meq/day, each level being maintained for 7-10 days. At the conclusion of each period at a given level of potassium intake, plasma potassium and excretion were measured and plotted, plasma potassium being the independent variable. Such a relationship was obtained while the dogs were on three different levels of sodium intake: 10, 100, and 200 meq/day. The curves from the data obtained at 100 and 200 meq/day sodium intake both were shifted to the left of the curve obtained at 10 meq/day (P less than 0.05), although the 100 and 200 meq/day curves were not different from each other. On the basis of these data one could predict that, at a plasma potassium concentration of 4.0 meq/liter, the animals would excrete potassium at a rate of 17 meq/day on a 10 meq/day sodium intake, 37 meq/day on a 100 meq/day sodium intake, and 47 meq/day on a 200 meq/day sodium intake. Urine flow and electrolyte concentration data are consistent with the hypothesis that the sodium intake effect on potassium excretion was mediated through increases in distal nephron flow rate and decreases in distal nephron potassium concentration.

Inhibition of aldosterone-induced antinatriuresis and kaliuresis by actinomycin D

1984 ◽  
Vol 246 (2) ◽  
pp. F201-F204 ◽  
Author(s):  
J. D. Horisberger ◽  
J. Diezi
Keyword(s):  
Urinary Excretion ◽  
Intravenous Infusion ◽  
Sodium Excretion ◽  
Actinomycin D ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Potassium Excretion ◽  
Short Term ◽  
Sodium And Potassium ◽  
Term Response

The effects of actinomycin D on short-term response to aldosterone on sodium and potassium urinary excretion were investigated in adrenalectomized glucocorticoid-substituted anesthetized rats. Aldosterone alone (1 microgram/kg followed by sustained intravenous infusion of 1 microgram X kg-1 X h-1) entailed a simultaneous antinatriuretic and kaliuretic effect after a latent period of 30-60 min. Actinomycin D (300 micrograms/kg) administered intravenously 30 min before aldosterone inhibited both the aldosterone-induced kaliuresis and antinatriuresis and the concomitant changes in plasma potassium concentration. The administration of actinomycin D alone enhanced sodium excretion in the first hour and then induced kaliuresis. These results favor the hypothesis that mineralocorticoid effects of aldosterone on sodium and potassium excretion are closely linked and may be dependent on the same mechanisms.

Cortisol-mediated synchrinization of circadian rhythm in urinary potassium excretion

1977 ◽  
Vol 233 (5) ◽  
pp. R230-R238 ◽  
Author(s):  
M. C. Moore-ede ◽  
W. S. Schmelzer ◽  
D. A. Kass ◽  
J. A. Herd
Keyword(s):  
Circadian Rhythm ◽  
Saimiri Sciureus ◽  
Potassium Excretion ◽  
Dark Cycle ◽  
Urinary Potassium ◽  
Timing System ◽  
Daily Dose ◽  
Circadian Timing System ◽  
Free Running ◽  
Renal Potassium Excretion

Conscious chair-acclimatized squirrel monkeys (Saimiri sciureus) studied with lights on (600 lx) from 0800 to 2000 h daily (LD 12:12) display a prominent circadian rhythm in renal potassium excretion. The characteristics of this rhythm were reproduced in adrenalectomized monkeys by infusing 5 mg cortisol and 0.001 mg aldosterone, or 5 mg cortisol alone, between 0800 and 0900 h daily. When the timing of cortisol adminisration (with or without aldosterone) was phase-delayed by 8 h, the urinary potassium rhythm resynchronized by 80% of the cortisol phase shift, but only after a transient response lasting 3–4 days. With the same daily dose of adrenal steroids given as a continuous infusion throughout each 24 h, urinary potassium excretion showed free-running oscillations no longer synchronized to the light-dark cycle. These results indicate that the cirdacian rhythm of plasma cortisol concentration acts as an internal mediator in the circadian timing system, synchronizing a potentially autonomous oscillation in renal potassium excretion to environmental time cues and to other circadian rhythms within the animal.

Effect of epinephrine on renal potassium excretion in the isolated perfused rat kidney

1984 ◽  
Vol 247 (2) ◽  
pp. F331-F338
Author(s):  
L. D. Katz ◽  
J. D'Avella ◽  
R. A. DeFronzo
Keyword(s):  
Rat Kidney ◽  
Fractional Excretion ◽  
Beta Agonist ◽  
Potassium Excretion ◽  
Isolated Perfused Rat Kidney ◽  
Beta Agonists ◽  
Beta Adrenergic Agonists ◽  
Urinary Potassium ◽  
Perfused Rat Kidney ◽  
Renal Potassium Excretion

The effects of beta-agonists (epinephrine, isoproterenol, and ITP) and beta-antagonists (propranolol, metoprolol, and butoxamine) on renal potassium excretion were examined using the isolated perfused rat kidney preparation. Following 30 min of control perfusion, one of the above beta-adrenergic agonists or antagonists was added to the perfusion medium. Following epinephrine, a combined beta 1- and beta 2-agonist, urinary potassium excretion (UKV; 0.55 +/- 0.55 vs. 0.36 +/- 0.04 mueq/min, P less than 0.001) and fractional excretion of potassium (FEK; 24.6 +/- 2.4 vs. 18.2 +/- 2.0%, P less than 0.001) both decreased. When isoproterenol, a nonspecific beta-agonist, was added to the perfusate, UKV (0.49 +/- 0.10 vs. 0.27 +/- 0.04 mueq/min, P less than 0.02) and FEK (29.0 +/- 5.2 vs. 16.3 +/- 2.9%, P less than 0.01) again decreased. ITP, a specific beta 1-agonist also caused a decrease in UKV (0.60 +/- 0.13 vs. 0.39 +/- 0.04 mueq/min, P less than 0.02) and FEK (30.2 +/- 5.1 vs. 17.8 +/- 2.8%, P less than 0.02). In contrast, when propranolol, a nonspecific beta-antagonist, was added to the perfusate, the opposite effects on renal potassium handling were observed. UKV (0.45 +/- 0.05 vs. 0.70 +/- 0.07 mueq/min, P less than 0.001) and FEK (23.0 +/- 2.1 vs. 42.5 +/- 3.1%, P less than 0.001) both increased. Metoprolol (50 ng/ml), a specific beta 1-antagonist, increased UKV (0.56 +/- 0.10 vs. 0.68 +/- 0.15 mueq/min, P less than 0.02) and FEK (31.0 +/- 3.8 vs. 48.0 +/- 7.1%, P less than 0.02). A similar effect was observed when a higher dose of metoprolol (200 ng/ml) was employed.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the renin-angiotensin system in potassium control

1980 ◽  
Vol 238 (5) ◽  
pp. R359-R363
Author(s):  
D. B. Young ◽  
R. E. McCaa
Keyword(s):  
Potassium Concentration ◽  
Renin Angiotensin System ◽  
Plasma Potassium ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Sodium ◽  
Group I ◽  
Urinary Potassium ◽  
Group Ii

To determine the importance of the renin-angiotensin system in control of plasma potassium concentration and excretion, potassium control was studied in two groups of dogs in response to a 20-fold increase in sodium intake (from 10 to 200 meq/day). Group I was intact whereas group II lacked feedback control of the renin-angiotensin system, which was eliminated by continuous infusion of 10 ng . kg-1 . min-1 angiotensin II. This rate of infusion reduced endogenous plasma renin activity (PRA) to undetectable levels throughout the study. The sodium forcing did not result in measurable changes in plasma potassium concentration or excretion in group I, in which PRA fell to 40% and plasma aldosterone concentration (PAC) to 60% of the low sodium levels. In group II the same sodium forcing produced a 12% decrease in plasma potassium concentration and a 79% increase in urinary potassium excretion. PAC also fell to 60% of the low sodium level in group II. The results demonstrate the importance of the renin-angiotensin system as a link between the nephron and the zona glomerulosa that is essential in controlling plasma potassium concentration and excretion during changes in sodium balance.

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