Relationship between plasma potassium concentration and renal potassium excretion

1982 ◽  
Vol 242 (6) ◽  
pp. F599-F603 ◽  
Author(s):  
D. B. Young

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.

1984 ◽  
Vol 246 (6) ◽  
pp. F772-F778 ◽  
Author(s):  
D. B. Young ◽  
T. E. Jackson ◽  
U. Tipayamontri ◽  
R. C. Scott

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.


1983 ◽  
Vol 244 (1) ◽  
pp. F28-F34 ◽  
Author(s):  
D. B. Young ◽  
A. W. Paulsen

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.


1987 ◽  
Vol 252 (1) ◽  
pp. F60-F64 ◽  
Author(s):  
L. Rossetti ◽  
G. Klein-Robbenhaar ◽  
G. Giebisch ◽  
D. Smith ◽  
R. DeFronzo

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).


1984 ◽  
Vol 66 (2) ◽  
pp. 129-140 ◽  
Author(s):  
K. E. Milmer ◽  
T. Bennett ◽  
S. M. Gardiner

1. Adrenal regeneration hypertension was induced in male Wistar rats by unilateral adrenal enucleation, contralateral adrenalectomy and the provision of a 1% (w/v) NaCl solution for drinking. 2. A fivefold increase in dietary KCl content caused a significant reduction in the systolic blood pressure of hypertensive rats but not of control rats. 3. During the increase in potassium intake there was a marked polydipsia. When 1% NaCl solution was the drinking fluid, the resultant increase in sodium intake was associated with an abolition of the antihypertensive effect of potassium loading, but when the sodium intake was held constant, the antihypertensive effect was maintained. 4. In rats with adrenal regeneration hypertension, plasma volume was significantly higher, and packed cell volume and plasma protein concentrations were significantly lower than in control rats. These differences were abolished after 4 days of dietary KCl supplementation. 5. Increased dietary potassium intake was associated with significantly lower serum aldosterone concentrations and significantly higher plasma potassium concentrations in adrenal enucleated rats compared with controls. 6. The possibility that a reduction in extracellular fluid volume (due to a natriuresis) and/or a peripheral vasodilatation contributed to the antihypertensive effect of KCl loading is discussed.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2345
Author(s):  
Masayuki Okuda ◽  
Satoshi Sasaki

The identification of sodium and potassium intake in youths is an important step to preventing the increase of blood pressure in childhood. We examined food intake and estimated mineral intake using a brief-type self-administered diet history questionnaire (BDHQ) to test its validity as a comparison with urinary excretion in Japanese youths. The subjects were 5th and 8th graders (n = 2377), who completed the BDHQ and permitted the use of their overnight urine specimens. Sodium intake was poorly associated with sodium excretion (Rho = 0.048), and the coefficients of dietary potassium and a sodium-to-potassium molar ratio were 0.091–0.130. Higher soybean paste (miso) intake and pickles were significantly associated with higher sodium excretion (p ≤ 0.005). However, these foods were positively associated with potassium excretion (p = 0.002–0.012), and not associated with an excreted sodium-to-potassium ratio. Fruits and dairy products were positively associated (p ≤ 0.048), whereas beverages were negatively associated with potassium excretion (p ≤ 0.004). The association of the sodium-to-potassium ratio was opposite to that of potassium (p ≤ 0.001). The choice of foods, potassium, and the sodium-to-potassium ratio assessed using the BDHQ are available as part of health education for youths, but the assessment of sodium intake in population levels should be carefully conducted.


1984 ◽  
Vol 246 (2) ◽  
pp. F201-F204 ◽  
Author(s):  
J. D. Horisberger ◽  
J. Diezi

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.


1976 ◽  
Vol 231 (3) ◽  
pp. 945-953 ◽  
Author(s):  
DB Young ◽  
RE McCaa ◽  
UJ Pan ◽  
AC Guyton

This study was conducted to determine the quantitative importance of the aldosterone feedback mechanism in controlling each one of three major factors that have often been associated with aldosterone, namely, extracellular fluid sodium concentration, extracellular fluid potassium concentration, and extracellular fluid volume. To do this, the ability of the body to control these three factors in the face of marked changes in daily sodium or potassium intake was studied under two conditions: 1) in the normal dog, and 2) in the dog in which the aldosterone feedback mechanism was prevented from functioning by removing the adrenal glands and then providing a continuous fixed level of supportive aldosterone and glucocorticoids during the low and high electrolyte intake periods. Under these conditions, removal of feedback control of aldosterone secretion decreased the effectiveness of plasma potassium control by nearly fivefold (39% vs. 8% change in plasma potassium concentration), fluid volume by sixfold (12% vs. 2% change in sodium space) and had no effect on control of plasma sodium concentration (2% change with and without feedback control of aldosterone secretion.)


1975 ◽  
Vol 38 (1) ◽  
pp. 163-170 ◽  
Author(s):  
M. C. Moore Ede ◽  
M. F. Brennan ◽  
M. R. Ball

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.


1965 ◽  
Vol 209 (6) ◽  
pp. 1219-1226 ◽  
Author(s):  
Helen Cserr

Potassium exchange between cerebrospinal fluid (CSF), plasma, and brain was investigated in anesthetized dogs and rats using the technique of ventriculocisternal perfusion. Transport via bulk secretion and absorption of CSF accounts for only 20% of total potassium exchange, unidirectional ionic fluxes across the ependyma for 80%. This large transependymal exchange is primarily between CSF and brain intracellular potassium pools, since two-thirds of the K42 outflux can be recovered from brain tissue. Conversely, much of transependymal influx comes from brain, as demonstrated by the low specific activity of influx relative to that of plasma following intravenous injection of K42. Potassium outflux is almost proportional to CSF [K+] in the range 0–10 mEq/liter but is independent of plasma [K+]. Perfusion with 10–5 m ouabain reduces transependymal K42 outflux to 25% of control; the residual outflux may be accounted for by passive processes. Results are discussed in terms of 1) regulation of CSF potassium concentration and 2) the relationship between CSF and brain extracellular fluid.


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