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Renal And Gastrointestinal Potassium Excretion In Humans: New Insight Based On New Data And Review And Analysis Of Published Studies

Hypertension Research Center of the Cardiovascular Research Institute of New Jersey (M.A., A.A.)
Department of Preventive Medicine and Community Health (J.D.B., F.W.K., W.L., J.S.), UMDNJ, New Jersey Medical School, Newark, New Jersey
USA Department of Agriculture, Agricultural Research Service, Grand Forks, Human Nutrition Research Center, Grand Forks, North Dakota (L.M.K.)
Department of Preventive Medicine and Community Health, University of Texas, Medical Branch Galveston, Texas (H.H.S.)

Address reprint requests to: John D. Bogden, PhD, Room F-506, Preventive Medicine & Community Health, UMDNJ, NJ Medical School, 185 South Orange Ave, Newark, NJ, 07103. E-mail: bogden{at}umdnj.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
Objectives: Little is known about the relationship between the renal and gastrointestinal excretion of potassium in humans. This information is important in light of strong associations of potassium intake with hypertension and occlusive stroke.

Methods: We determined the relationship between fecal and urinary excretion of potassium under both fixed and variable potassium intakes using our unpublished archival data and published data of others. Twenty-five subjects were evaluated.

Results: On a fixed, low oral potassium intake (61.2 ± 4.7 mmol/day; mean ± SD), there was an inverse relationship between fecal and urinary potassium excretion (r = –0.66, p = 0.040). In studies in which potassium intake varied between 61–135 mmol/day, fecal and urinary potassium excretions were positively correlated (r = 0.58, p = 0.024). Considerable within-and-between-subject variation was observed in the relationship between fecal and urinary potassium excretion.

Conclusions: Inter-individual variation in fecal potassium excretion may arise from both variation in dietary potassium intake and intrinsic individual differences in the renal versus gastrointestinal handling of potassium.

Key words: potassium, steady-state, kidney, intestine, urine, feces

	INTRODUCTION

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Epidemiologic studies have documented a strong association between potassium intake and not only blood pressure [1,2], but also occlusive stroke [3–6]. The cardiovascular effects of dietary potassium may hence be mediated through both blood pressure independent and dependent mechanisms.

Given the potential impact of dietary potassium on cardiovascular disease, it is surprising that relatively little is known about the relationship between renal and gastrointestinal excretion of potassium in humans. Urinary potassium excretion largely reflects potassium intake, but the question as to how much of the oral intake of potassium is excreted via the gastrointestinal tract versus the kidneys has not been addressed systematically. This question is important for several reasons. First, potassium intake is routinely estimated from the urinary output. However, if considerable variation exists among subjects in fecal potassium excretion, the urinary excretion of potassium may not provide an accurate account of potassium intake in individuals with a relatively high fecal potassium excretion. Second, as a group, African-Americans excrete less urinary potassium than do Whites [7–16]. This has been attributed, without adequate substantiation, to low potassium intake in African-Americans. In principle, racial differences in urinary potassium excretion may not necessarily relate only to oral intake but also to variation in fecal excretion of potassium [17–19]. Third, the fecal/urinary potassium excretion in response to increased potassium intake might affect clinical response. For these reasons, it is essential to know the contributions of the gastrointestinal tract and the renal system to overall potassium balance over a range of potassium intakes.

Our main hypothesis was that on constant potassium intake, fecal potassium is inversely correlated with urinary potassium. The logic behind this argument is that to maintain a steady state of potassium, individuals excreting less urinary potassium must excrete more fecal potassium. We also anticipated, as has already been shown [20], that urinary and fecal potassium contents increase proportionally to oral potassium intake.

We proceeded in two phases: For phase 1, we reviewed archival data from our metabolic studies in which a moderately low potassium intake was held constant. For phase 2, we reviewed published data on metabolic studies documenting the urinary and fecal excretion of potassium on what is considered a normal range of potassium intakes. In this way, we were able to determine the relationship between urinary and gastrointestinal potassium excretion and their relative contributions to overall potassium homeostasis in humans. We note that Agarwal et al [20], have reviewed studies of potassium excretion, but did not provide a comprehensive picture from which one can clearly deduce the relationship between urinary and fecal potassium over a wide range of potassium intakes.

	MATERIALS AND METHODS

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Phase 1
These metabolic studies were performed by two of the authors (L. M. Klevay and H.H. Sandstead) and co-workers between 1981 and 1983. Volunteers were selected after extensive evaluations for physical and psychological health. Subjects ate a diet of conventional food, adequate in all nutrients except when dietary zinc was decreased for evaluation of its effect on trace element physiology. Food was consumed quantitatively, none from external sources. Energy equilibrium was attained by individualizing diet and exercise prescriptions. Physical fitness was maintained. Feces and urine were collected quantitatively.

The subjects of the Phase 1 studies were 10 healthy White males with the following characteristics: age = 34 ± 13.8 (mean ± SD) years, height = 172 ± 4.8 cm, weight 69.7 ± 5.4 kg (BMI = 23.7 ± 2.55 kg/m²). They were admitted to a metabolic ward and over the course of roughly one half year underwent between 8–39 balance studies, each of 3 or 6 days duration, for a total number of 225 balance studies. Of these, 6 were 3-day balance periods and 219 were 6-day balance periods. Studies were performed to assess various aspects of trace metal and carbohydrate metabolism [21–24]. Confinement of subjects to a metabolic ward ensured compliance with quantitative food consumption and the completeness of urine and feces collections.

Potassium was measured by inductively coupled argon plasma spectroscopy [25], following destruction of organic matter of freeze-dried material with nitric and perchloric acids [26,27]. To monitor the reproducibility of the fecal potassium analysis, a pooled fecal sample was prepared and aliquots of this sample analyzed at regular intervals with each set of determinations over a one-year period. A total of 13 analyses of this sample were performed. The relative SD for these data was 4.79%, suggesting high reproducibility of the analytical method for fecal potassium. For our analysis we used the data on potassium intake and excretion during consumption of the basal (zinc intake 8.8 ± 1.2 mg/day), low zinc (3.2 ± 0.24), and high zinc (32.2 ± 0.6 mg/day) diets. To assess daily potassium intake, duplicate diets were prepared for each subject. These diets were blended and analyzed to provide the daily potassium intake for each subject. Diets provided 61.2 ± 4.7 mmol potassium per day and 117.3 ± 32.6 mmol sodium per day. Table 1 shows that there was no effect of oral zinc manipulation on urinary and fecal potassium excretion, and, therefore, all data were pooled for analysis.

Phase 2
Although there are many publications with data on urinary potassium, data on fecal potassium obtained in concert with measurements of urinary potassium are infrequent. The few articles (n = 5) with both urinary and fecal potassium data on the same individuals under controlled conditions are considered here. These studies were identified using a "PubMed" search and by examining references cited in the review paper by Agarwal et al [20]. The 5 studies were published between 1948 and 1958 and they involved a total of fifteen normal subjects whose potassium excretions were analyzed in both urinary and fecal specimens collected for periods of 3–7 days [28–32]. These studies include a variety of experimental manipulations, but here we present data from control periods or periods that involved potassium supplements. Neither Agarwal et al. [20], nor the more recent publication on Dietary Reference Intakes for potassium (http://www.nap.edu/books/0309091691/html/) provided other data usable for the current study. The daily urinary and stool excretions were computed based on the overall study duration divided by the number of days of each collection period. Some subjects underwent a number of periods of collections. Dietary potassium intake was estimated to be 61–135 mmol/day based on the combined excretion of urinary and fecal potassium (assuming that the loss of potassium through sweat, respiration and other routes was minimal). In two studies [27,28], potassium supplementation was in the form of both KCl and KHCO₃. No phase 2 study indicated the race of the subjects. Two studies did not indicate the gender of the subjects [28,29]. Subjects in the remaining studies comprised either males [29,32], or males and a female [31]. Age, documented in three studies, ranged between 20 and 30 years. Flame photometry [33] was used for the measurement of potassium in all phase 2 studies.

Although the method for potassium measurement in studies described under phase 2 differed from that in phase 1, both methods have had extensive validation.

Statistical Analysis
In both phases, the fecal and urinary potassium excretion of each subject was summarized as the mean of the individual's daily fecal potassium excretion and the mean of urinary potassium excretion across the available balance studies. The individual means of daily urinary potassium excretion were then regressed linearly on the means of daily fecal potassium excretion values, inversely weighted by the number of balance studies. For descriptive purposes, we also performed unweighted correlation analyses using all daily excretion data available for each subject. These data are presented in insets of figures 2 and 4. Two-tailed p values are reported to indicate the level of statistical significance based on weighted correlation coefficients.

View larger version (25K): [in this window] [in a new window]   Fig. 2. The relationship between fecal and urinary potassium excretion of 10 subjects on a fixed potassium intake of 61.2 ± 4.70 mmol/day (Phase 1). The main figure depicts mean values, presented with weighted linear regression line, weighted correlation coefficient and p value. Horizontal lines within the main figure are standard error bars for fecal potassium excretion and vertical lines are standard error bars for urinary potassium excretion. The inset presents all observations. Each of the 10 subjects in the inset was assigned a different symbol that is identical to the symbol used for the subject in the main figure. The linear regression line based on multiple observations per individual and r (Pearson correlation coefficient) and p value of the linear regression are noted.

View larger version (22K): [in this window] [in a new window]   Fig. 4. The relationship between fecal and urinary potassium excretion of subjects maintained on a variable potassium intake of 61–135 mmol/day (Phase 2). The main figure depicts mean values, presented with weighted linear regression line, weighted correlation coefficient and p value. The numbers above the points in the main figure are mmole/day of dietary potassium ingested by the subject; these values are provided for 12 of the 15 Phase 2 study subjects. Corresponding data for the remaining 3 subjects were not available. The Arrow denotes 2 coincident superimposed data points. The inset presents all observations. Each of the 15 subjects in the inset is assigned a different symbol, the same symbol used for that subject in the main figure. The linear regression line based on multiple observations per subject and r (Pearson correlation coefficient) and p value of the linear regression are noted.

	RESULTS

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Fig. 1 summarizes the intra and inter-individual variability in the daily fecal/urinary and in the fecal otal (fecal plus urinary) potassium excretions. There was considerable variation among subjects in the relationship between urinary and fecal potassium excretions. Fig. 2 shows a negative correlation between urinary and fecal potassium excretion on the fixed potassium intake. Individuals excreting less potassium in the urine were correspondingly excreting more fecal potassium. The weighted linear regression describing this relation is: y = 56.5 – 0.813x, where y is the urinary excretion and x the fecal excretion of potassium in units of mmol/day.

View larger version (14K): [in this window] [in a new window]   Fig. 1. Inter and intra-individual variability in fecal/urinary potassium and fecal otal (urinary + fecal) potassium excretion ratios for the 10 subjects of Phase 1 (fixed potassium intake) of the study. Subjects were stratified in descending order by the mean (horizontal lines) of the fecal/urinary potassium excretion ratio expressed as a percentage.

View larger version (12K): [in this window] [in a new window]   Fig. 3. Inter and intra-individual variability in fecal/urinary potassium and fecal otal (urinary + fecal) potassium excretion ratios for phase 2 (variable potassium intake) of the study. Subjects were stratified in descending order by the mean (horizontal lines) of the fecal/urinary potassium excretion ratio expressed as a percentage.

View larger version (18K): [in this window] [in a new window]   Fig. 5. Convergence of the linear regressions describing the relationships between fecal and urinary potassium excretions in phases 1 and 2 to a similar threshold of urinary potassium excretion (56.5–62.6 mmol/day). Dashed lines are extrapolations beyond the lowest data point for fecal and urinary potassium excretions. The threshold is a mean value reflecting inter-individual variation in the relationship between fecal and urinary potassium excretion. Above the threshold, a positive relation exists between fecal and urinary potassium excretions. Below the threshold, there is a robust negative correlation between fecal and urinary potassium excretions when subjects are maintained on a fixed potassium intake.

	DISCUSSION

Phase 2 of the study showed that in absolute terms, the gastrointestinal tract contributed considerably to the overall potassium loss as potassium intake increased. A study, performed in potassium-supplemented athletes under various circumstances, supports this finding by showing that fecal potassium excretion was between 21–24% of urinary potassium excretion [34]. However, our phase 1 results provided another important insight, which, although self-evident, has never been shown; for a given potassium intake, individuals who excreted less potassium in the urine excreted more potassium in the feces. From the standpoint of overall potassium balance, this relationship makes biological sense. Assuming that sweat, respiratory and other potassium losses are minimal, the combined fecal and urinary excretion of potassium should approximate oral intake. We must underscore, nonetheless, that our conclusions are derived from a total of twenty-five, primarily male subjects who were known to be (phase 1) or most likely to be (phase 2) Whites.

Regardless of the mechanisms that account for the fecal excretion of potassium, namely, absorption in the upper intestinal tract, secretion in the lower intestinal tract, shedding of epithelial cells from the intestinal lumen, or any combination of these factors (reviewed in 20 and 35), it is evident that the intestine contributes substantially but with considerable inter- and intra- subject variability to overall potassium loss in normal humans. Because aldosterone may influence sodium and potassium excretion, fluctuations in aldosterone levels may in part account for this variability (35).

Given that the lowest amount of mean daily fecal excretions for individuals in phases 1 and 2 were 5 and 2 mmol/day, respectively, values in this range may provide a good estimate of the minimum value of daily fecal potassium excretion. We note that such extrapolations are meaningful when individuals are in potassium balance. However, obligatory fecal and urinary potassium losses during potassium depletion (28) may not maintain the same relationship as when potassium intake is sufficient to hold body potassium at steady-state, as in the current study.

When extrapolated to a fecal potassium excretion of zero (Fig. 5), the weighted linear regressions describing the relations between fecal and urinary potassium excretion yielded values of 56.5 and 62.6 mmol/day for daily urinary potassium excretion for Phases 1 and 2, respectively. Thus, despite the heterogeneity of the individual Phase 2 studies, when plotted and extrapolated to a fecal potassium excretion of zero they provide a value for daily urine excretion very similar to the Phase 1 Study. These findings suggest that the threshold for fecal excretion of potassium is about 55–60 mmol/day of oral intake. Although drawing conclusions from the heterogenous studies of Phase 2 must be done with caution, 55–60 mmol/day may also be the minimal daily potassium requirement in White adults. As dietary potassium increases above this range, there is the expected positive association between fecal and urinary potassium excretion. In contrast below the threshold intake of 55–60 mmole/day conservation of body potassium appears to be maintained by reduced urinary potassium excretion at higher levels of fecal excretion and/or reduced fecal excretion at higher levels of urinary excretion, as shown in Fig. 5. This inverse relationship between urinary and fecal excretion is an inevitable consequence of the steady-state (zero balance) that appears to be maintained in our subjects at intakes of 55–60 mmole/day. This is a very logical system that could help to conserve body potassium stores at low intakes.

There are a number of important ramifications of these findings. Estimation of potassium intake based on urinary potassium excretion may not be accurate due to variation among individuals in the gastrointestinal handling of potassium. Moreover, whatever the mechanisms whereby high potassium intake reduces cardiovascular risks, a variable outcome of raising potassium intake on such risks may be anticipated not only because of differences in the target organ responses to oral potassium but also due to differences in the renal and/or gastrointestinal handling of the ion among subjects. We note, however, that our findings provide no information about whether the inverse relationship between urinary and gastrointestinal excretion of potassium at constant intake arises from primary variation in the renal excretory capacity of potassium, leading to a secondary adaptation in the gastrointestinal excretion, or vice versa, so that a potassium steady-state is maintained. This concept is also applicable to the differences between African-Americans and Whites in urinary potassium excretion.

What is puzzling about the lower urinary potassium excretion in African-Americans than in Whites is that multiple investigators have noted this phenomenon in various USA populations dating back more than a quarter of a century [7–16]. In one study fecal and urinary potassium excretions were measured in a small group comprising 7 African-Americans and 6 Whites [11]. Based on a self-administered food inventory, it was estimated that potassium intake was lower in African-Americans than Whites. On their habitual intake and after ingesting potassium-supplements, African-Americans excreted less urinary potassium than Whites. The ratio between fecal and urinary potassium excretion while on the habitual dietary intake was 0.23 in Whites and 0.30 in African-Americans. Insufficient information was provided in this study to assess fecal/urinary excretion ratios during the period of potassium supplementation. In another study of a small cohort of Black and White South Africans it was found, based on the combined excretion of urinary and fecal potassium, that the potassium intake was considerably lower in Black than in White South Africans [35]. However, the ratio of the fecal to urinary excretion of potassium was 0.39 in Black compared with 0.26 in White South Africans. Thus, for a given potassium intake, it appears that both African-Americans and Black South Africans excreted proportionally more potassium via the gastrointestinal tract than did Whites.

Voors [11], Langford [14], Kimura [16] and co-workers found lower urinary potassium excretion in African-Americans than in Whites under basal conditions and after potassium chloride dietary supplements. The conclusion of Voors [11], Langford [14] and their co-workers were that their findings were indicative of a chronic deficit in body potassium due to habitually lower potassium intake in African-Americans than Whites. If so, total body potassium load should be lower in African-Americans than in Whites; however, a recent study of a large sample of subjects found that total body potassium corrected for weight and height is actually higher but declines more rapidly with age in African-Americans than in Whites [37]. We, therefore, propose that differences between African- Americans and Whites in urinary potassium excretion are not solely the reflection of racial differences in potassium intake and theoretically may be explained, at least in part, by higher gastrointestinal potassium excretion in Blacks.

Collectively, differences in urinary potassium excretion between African-Americans and Whites suggest racial variation in the renal/gastrointestinal handling of potassium so that for a given potassium intake, African-Americans maintain steady-state by excreting relatively less urinary and relatively more fecal potassium than Whites. Such an assumption seems reasonable considering the well-documented racial differences in the renal handling of sodium [37–41]—an ion whose metabolism is closely linked to that of potassium.

We suggest that research exploring inter-individual, as well as race, gender, and age related variations in the relationship between gastrointestinal and renal handling of potassium is warranted to better understand the impact of potassium intake on cardiovascular risk in humans. Another important line of inquiry may be to relate renal function to the gastrointestinal excretion of potassium.

	ACKNOWLEDGMENTS

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This project was funded by NHLBI grant RO1 HL-47906 and the Healthcare Foundation of New Jersey. M. Aladjem contributed to this work while on a sabbatical leave from the Assaf Harofe Medical Center, The Sackler School of Medicine, Tel-Aviv University.

Received March 31, 2005. Accepted May 3, 2006.

	REFERENCES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 

1. Gallen IW, Rosa RM, Esparaz DY, Young JB, Robertson GL, Batlle D, Epstein FH, Landsberg L: On the mechanism of the effects of potassium restriction on blood pressure and renal sodium retention.Am J Kidney Dis31 :19 –27,1998 .[Medline]
2. Whelton PK, He J, Cutler JA, Brancati FL, Appel LJ, Follmann D, Klag MJ: Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials.JAMA277 :1624 –1632,1997 .[Abstract/Free Full Text]
3. Ascherio A, Rimm EB, Hernan MA, Giovannucci EL, Kawachi I, Stampfer MJ, Willett WC: Intake of potassium, magnesium, calcium and fiber and risk of stroke among US men.Circulation98 :1198 –1204,1998 .[Abstract/Free Full Text]
4. Iso H, Stampfer MJ, Manson JE, Rexrode K, Hennekens CH, Colditz GA, Speizer FE, Willett WC: Prospective study of calcium, potassium and magnesium intake and risk of stroke in women.Stroke30 :1772 –1779,1999 .[Abstract/Free Full Text]
5. Green DM, Ropper AH, Kronmal RA, Psaty BM, Burke GL: Cardiovascular Health Study. Serum potassium level and dietary potassium intake as risk factors for stroke.Neurology59 :314 –320,2002 .[Abstract/Free Full Text]
6. Khaw KT, Barrett-Connor E: Dietary potassium and stroke-associated mortality. A 12 year prospective population study.N Engl J Med316 :235 –240,1987 .[Abstract]
7. Luft FC, Rankin LI, Bloch R, Weyman AE, Willis LR, Murray RH, Grim CE, Weinberger MH: Cardiovascular and humoral responses to extremes of sodium intake in normal black and white men.Circulation60 :697 –706,1979 .[Free Full Text]
8. Berenson GS, Voors AW, Dalferes ER Jr, Webber LS, Shuler SE: Creatinine clearance, electrolytes and plasma renin activity related to the blood pressure of white and black children—the Bogalusa heart study.J Lab Clin Med93 :535 –548,1979 .[Medline]
9. Watson RL, Langford HG, Abernethy J, Barnes TY, Watson MJ: Urinary electrolytes, body weight, and blood pressure. Pooled cross-sectional results among four groups of adolescent females.Hypertension2 :93 –98,1980 .[Medline]
10. Voors AW, Berenson GS, Shuler SE, Webber LS: Blood pressure, electrolyte clearance, and plasma renin activity in children sampled from an entire community.J Applied Biochem2 :87 –99,1980 .
11. Voors AW, Dalferes ER Jr, Frank GC, Aristimuno GG, Berenson GS: Relation between ingested potassium and sodium balance in young Blacks and whites.Am J Clin Nut37 :583 –594,1983 .[Abstract/Free Full Text]
12. Lasker N, Hopp L, Grossman S, Bamforth R, Aviv A: Race and sex differences in red blood cell Na, K and Na-K-ATPase.J Clin Invest75 :1813 –1820,1985 .[Medline]
13. Pratt JH, Jones JJ, Miller JZ, Wagner MA, Fineberg NS: Racial differences in aldosterone excretion and plasma aldosterone concentrations in children.N Engl J Med321 :1152 –1157,1989 .[Abstract]
14. Langford HG, Cushman WC, Hsu H: Chronic effect of KCI on black-white differences in plasma renin activity, aldosterone, and urinary electrolytes.Am J Hypertens4 :399 –403,1991 .[Medline]
15. Pratt JH, Ambrosius WT, Agarwal R, Eckert GJ, Newman S: Racial difference in the activity of the amiloride-sensitive epithelial sodium channel.Hypertension40 :903 –908,2002 .[Abstract/Free Full Text]
16. Kimura M, Lu X, Skurnick J, Awad G, Bogden J, Kemp F, Aviv A: Potassium chloride supplementation diminishes platelet reactivity in humans.Hypertension44 :969 –973,2004 .[Abstract/Free Full Text]
17. Suh A, DeJesus E, Rosner K, Lerma E, Yu W, Young JB, Rosa RM: Racial differences in potassium disposal.Kidney Int66 :1076 –1081,2004 .[Medline]
18. Delgado-Almedia A: Reinterpreting sodium-potassium data in salt-sensitivity hypertension: A prospective debate.Hypertension45 :e4 ,2005 .[Free Full Text]
19. Aviv A, Hollenberg NK, Weder A: Urinary potassium excretion and sodium sensitivity in blacks. Response to reinterpreting sodium-potassium data in salt-sensitivity hypertension: A prospective debate.Hypertension45 :e4 –5,2005 .[Free Full Text]
20. Agarwal R, Afzalpurkar R, Fordtran JS: Pathophysiology of potassium absorption and secretion by the human intestine.Gastroenterology107 :548 –571,1994 .[Medline]
21. Klevay LM, Inman L, Johnson LK, Lawler M, Mahalko JR, Milne DB, Lukaski HC, Bolonchuk W, Sandstead HH: Increased cholesterol in plasma in a young man during experimental copper depletion.Metabolism33 :1112 –1118,1984 .[Medline]
22. Lykken GI, Mahalko J, Johnson PE, Milne D, Sandstead HH, Garcia WJ, Dintzis FR, Inglett GE: Effect of browned and unbrowned corn products intrinsically labeled with ⁶⁵Zn on absorption of ⁶⁵Zn in humans.J Nutrit116 :795 –801,1986 .[Abstract/Free Full Text]
23. Munoz JM, Sandstead HH, Jacob RA: Effects of dietary fiber on glucose tolerance of normal men.Diabetes28 :496 –502,1979 .[Medline]
24. Johnson PE, Lykken GI: Copper-65 absorption by men fed intrinsically and extrinsically labeled whole wheat bread.J Agricult Food Chem36 :537 –540,1988 .
25. Greenfield S, Jones IU, Berry CT: Inductively coupled argon plasma spectroscopy.Analyst89 :713 –720,1964 .
26. Anon B: Methods for the destruction of organic matter.Analytical Methods Committee Analyst85 :643 –656,1960 .
27. Smith GF: Wet oxidation of organic matter employing perchloric acid at graded oxidation potentials and controlled temperatures.Analytica Chimica Acta17 :175 –185,1957 .
28. Black DAK, Milne MD: Experimental potassium depletion in man.Clin Sci11 :397 –415,1953 .
29. Squires RD, Huth EJ: Experimental potassium depletion in normal human subjects. I. Relation of ionic intakes to the renal conservation of potassium.J Clin Invest38 :1134 –1148,1959 .[Medline]
30. August JT, Nelson DH, Thorn GW: Response of normal subjects to large amounts of aldosterone.J Clin Invest37 :1549 –1555,1958 .[Medline]
31. Relman AS, Schwartz WB: The effect of DOCA on electrolyte balance in normal man and its relation to sodium chloride intake.Yale J Biol Med24 :540 –558,1952 .[Medline]
32. Deitrick JE, Whedon GD, Shorr E: Effects of immobilization upon various metabolic and physiologic functions of normal men.Am J Med4 :3 –36,1948 .[Medline]
33. Wallace WM, Holiday M, Cushman M, Elkington JR: The application of the internal standard flame photometer to the analysis of biologic material.J Lab Clin Med37 :621 –629,1951 .[Medline]
34. Zorbas YG, Kakurin VJ, Kuznetsov NA, Yarullin VL, Andreyev ID, Charapakhin KP: Measurements in potassium-supplemented athletes during and after hypokinetic and ambulatory conditions.Biol Trace Elem Res85 :1 –22,2002 .[Medline]
35. Kunzelmann K, Mall M: Electrolyte transport in the mammalian colon: mechanisms and implications for disease.Physiol Rev82 :245 –289,2002 .[Abstract/Free Full Text]
36. Barlow RJ, Connell MA, Milne FJ: A study of 48-hour faecal and urinary electrolyte excretion in normotensive black and white South African males.J Hypertens4 :197 –200,1986 .[Medline]
37. He Q, Heo M, Heshka S, Wang J, Pierson RN Jr, Albu J, Wang Z, Heymsfield SB, Gallagher D: Total body potassium differs by sex and race across the adult age span.Am J Clin Nutr78 :72 –77,2003 .[Abstract/Free Full Text]
38. Price DA, Fisher ND: The renin-angiotensin system in blacks: active, passive, or what?Curr Hypertens Rep5 :225 –230,2003 .[Medline]
39. Aviv A: Cellular calcium and sodium regulation, salt-sensitivity and essential hypertension in African Americans.Ethn and Health1 :275 –281,1996 .
40. Weinberger MH: Racial differences in renal sodium excretion: relationship to hypertension.Am J Kidney Dis21 :41 –45,1993 .[Medline]
41. Aviv A, Hollenberg NK, Weder A: Urinary potassium excretion and sodium sensitivity in blacks.Hypertension43 :707 –713,2004 .[Abstract/Free Full Text]

This Article Abstract Figures Only Full Text (PDF) Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Klevay, L. M. Articles by Aviv, A. Search for Related Content PubMed PubMed Citation Articles by Klevay, L. M. Articles by Aviv, A.