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Background: The link between acid-base homeostasis and skeletal integrity has gained increasing prominence in the literature. Estimation of the net rate of endogenous noncarbonic acid production (NEAP) from dietary protein and potassium content enables exploration of the effects of dietary acidity or alkalinity on bone. Objective: The study aimed to ascertain whether lower dietary acidity (lower dietary protein intake but higher potassium intake--ie, low estimate of NEAP) was associated with greater axial and peripheral bone mass and less bone turnover, independent of key confounding factors. Design: Baseline (cross-sectional) results of a population-based study were examined further. The database includes spine and hip bone mineral density (BMD) in 1056 premenopausal or perimenopausal women aged 45-54 y and forearm bone mass and the urinary markers of bone resorption in 62 women. A validated food-frequency questionnaire was used to measure dietary intakes. Results: Lower estimates of energy-adjusted NEAP were correlated with greater spine and hip BMD and greater forearm bone mass (P < 0.02 to P < 0.05). Hip and forearm bone mass decreased significantly across increasing quartiles of energy-adjusted NEAP (P < 0.02 to P ,< 0.03), and trends at the spine were similar (P < 0.09). Differences remained significant after adjustment for age, weight, height, and menstrual status. Lower estimates of energy-adjusted NEAP were also correlated with lower excretion of deoxypyridinoline and were significant predictors of spine and forearm bone mass. Conclusions: These novel findings provide evidence of a positive link between a ratio of lower protein to higher potassium dietary intake (ie, less dietary acid) and skeletal integrity. Am J Clin Nutr 2004;79:131-8. KEY WORDS Bone health, potassium, protein, dietary acid, dietary alkali, acid-base homeostasis

Background: A substantial proportion of total body potassium (TBK) in humans is found in skeletal muscle (SM), thus affording a means of predicting total-body SM from whole-body counter-measured [sup.40]K. There are now > 30 whole-body counters worldwide that have large cross-sectional and longitudinal TBK databases. Objective: We explored 2 SM prediction approaches, one based on the assumption that the ratio of TBK to SM is stable in healthy adults and the other on a multiple regression TBK-SM prediction equation. Design: Healthy subjects aged [greater than or equal to] 20 y were recruited for body-composition evaluation. TBK and SM were measured by whole-body [sup.40]K counting and multislice magnetic resonance imaging, respectively. A conceptual model with empirically derived data was developed, to link TBK and adipose tissue--free SM as the ratio of TBK to SM. Results: A total of 300 subjects (139 men and 161 women) of various ethnicities with a mean ([+ or -] SD) body mass index (in kg/[m.sup.2]) of 25.1 [+ or -] 5.4 met the study entry criteria. The mean conceptual model--derived TBK-SM ratio was 122 mmol/kg, which was comparable to the measurement-derived TBK-SM ratios in men and women (119.9 [+ or -] 6.7 and 118.7 [+ or -] 8.4 mmol/kg, respectively), although the ratio tended to be lower in subjects aged [greater than or equal] 70 y. A strong linear correlation was observed between TBK and SM (r = 0.98, P < 0.001), with sex, race, and age as small but significant prediction model covariates. Conclusions: Two different types of prediction models were developed that provide validated approaches for estimating SM mass from [sup.40]K measurements by whole-body counting. These methods afford an opportunity to predict SM mass from TBK data collected in healthy adults. KEY WORDS Body composition, nutritional assessment, whole-body counting, total body potassium, skeletal muscle, prediction models, ratio of total body potassium to skeletal muscle

Background: Total body potassium (TBK) is known to decline throughout adulthood. The relations between physical activity, age, anabolic hormones, and TBK have rarely been considered. Objective: We sought to describe the relation between habitual physical activity, age, serum estradiol, and insulin-like growth factor I (IGF-I) and TBK in postmenopausal women. Design: TBK, fat-free mass (FFM), moderate-to-vigorous-intensity physical activity (MVPA; assessed with use of a semistructured interview), and serum concentrations of estradiol, IGF-I, and IGF binding protein 3 (IGFBP-3) were quantified in 51 healthy white women aged 54-76 y. Results: The potassium content of FFM declined curvilinearly with age, indicating an accelerated loss of skeletal muscle after 65 y of age. With the data split into high (n = 25) and low (n = 26) MVPA groups, the active women had 6.5% more potassium per FFM than did their less-active counterparts (P < 0.01). In multiple regression analysis, MVPA was the major determinant of the potassium content of FFM (P = 0.02), such that an active 70-y-old had the potassium content value of a 55-y-old sedentary woman. Serum estradiol, IGF-I, and IGFBP-3 were not significant determinants of the potassium content of FFM. Conclusions: These data suggest that 1) habitual physical activity can significantly influence FFM potassium content; 2) physical activity must, therefore, be considered if the effect of aging per se on TBK is to be clarified; and 3) MVPA, such as that pursued by the active women in the present study (eg, walking, dancing, floor exercises, and swimming), can assist in preventing sarcopenia in older women. KEY WORDS Total body potassium, fat-free mass, physical activity, aging, postmenopausal women, estradiol, insulin-like growth factor I, sarcopenia

Objective: To study the effect of intravenous (IV) terbutaline on potassium (K) and magnesium (Mg) distribution, ECG changes, and prevalence of ventricular ectopic beats in healthy subjects. Design: Randomized double-blind, [...]

There are conflicting data regarding the impact of serum potassium and magnesium levels on susceptibility to ventricular premature complexes (VPCs) in the clinical setting, The associations of serum potassium and magnesium levels with the prevalence of complex or frequent (>30/hour, multiform or repetitive) VPCs were examined after adjusting for age, sex, smoking, caffeinated coffee consumption, alcohol consumption, and left ventricular mass in Framingham Offspring Study subjects who were free of clinically apparent heart disease. There were 3,327 eligible subjects (mean age 44 years). Complex or frequent VPCs were present in 183 subjects (5.5%). When age-adjusted prevalences of complex or frequent VPCs were compared among quartiles of serum potassium and magnesium using a trend test, lower potassium (p = 0.002) and lower magnesium (p = 0.010) levels were associated with higher prevalence rates of arrhythmia. In logistic regression analyses that included potassium and magnesium simultaneously, potassium (p = 0.0021) and magnesium (p = 0.0311) levels were inversely associated with the occurrence of complex or frequent VPCs after adjustment for age, sex, smoking, coffee and alcohol consumption, diuretic use, and systolic blood pressure. These associations remained significant after accounting for left ventricular mass. A 1 SD decrement in potassium (0.48 mEq/liter) or magnesium (0.16 mEq/liter) level was associated with a 27% (95% confidence interval 6% to 51%) and a 20% (95% confidence interval 3% to 41%) greater odds of complex or frequent VPCs, respectively. Lower levels of serum potassium and magnesium were concurrently associated with higher prevalence rates of ventricular arrhythmias. (Am J Cardiol 1994;74-232-235)

A fraction from normal human plasma inhibiting [Na.sup.+] -[K.sup.+] ATPase has been recently identified as lysophosphatidylcholine (LPC). The aim of this study was to investigate the existence of a relationship [...]

* Objective: To determine the effect of trimethoprim-sulfamethoxazole (Tmp-Smx) on serum potassium concentration. * Design: Retrospective cohort study. * Setting: An urban teaching hospital. * Patients: Fifty-one persons hospitalized for symptomatic infection with human immunodeficiency virus (HIV). Twenty-five patients who were taking high-dose Tmp-Smx (trimethoprim 20 mg/kg per day; sulfamethoxazole, 100 mg/kg per day) for Pneumocystis carinii pneumonia were the study group. Twenty-six patients who had not received the drug were the control group. Patients who received potassium supplements, those taking medications known to alter potassium homeostasis or renal function, or those with a serum creatinine level more than 186 [Mu] mol/L were excluded. * Measurements and Main Results: Serum potassium concentration in the study group was 4.1 [+ or -] 0.1 mmol/L (mean [+ or -] SE) and increased by 1.1 mmol/L (Cl, 0.8 to 1.5 mmol/L) (P < 0.0001) 9.8 [+ or -] 0.5 days after starting Tmp-Smx therapy. Patients followed longitudinally showed a progressive increase in serum potassium levels during therapy and a progressive decline after discontinuing Tmp-Smx. Blood urea nitrogen and serum creatinine levels increased mildly from 4.3 [+ or -] 0.5 mmol/L and 85 [+ or -] 6 [m u] mol/L to 6.4 [+ or -] 0.7 mmol/L and 113 [+ or -] 8 [m u] mol/L, respectively. The serum potassium level in the control group was 4.3 [+ or -] 0.1 mmol/L and remained unchanged during hospitalization. * Conclusions: High-dose Tmp-Smx therapy used for the treatment of P. carinii pneumonia in HIV-infected patients leads to an increase in the serum potassium concentration and may result in life-threatening hyperkalemia. Patients receiving high doses of Tmp-Smx require close monitoring of their serum potassium concentration, particularly 7 to 10 days after the start of therapy., Treatment with high-dose trimethoprim-sulfamethoxazole (Tmp-Smx) for Pneumocystis carinii pneumonia may cause hyperkalemia in patients with HIV infection. Hyperkalemia is abnormally high blood levels of potassium. Among 51 patients hospitalized for HIV infection, 25 were treated with high-dose Tmp-Smx for P. carinii pneumonia and 26 were not been treated with Tmp-Smx (control group). Blood levels of potassium were similar in the two groups of patients before treatment with Tmp-Smx was begun. Potassium concentration increased progressively during treatment with Tmp-Smx among members of the treatment group, but declined after treatment was discontinued. Blood levels of potassium remained the same in patients from the control group. Patients treated with high-dose Tmp-Smx should be monitored closely for increases in their blood levels of potassium.

Although the hypokalemic effect of inhaled [[unkeyable].sup.2]-adrenergic agonists has been well documented, little is known as to their effect on plasma magnesium. We therefore examined in ten healthy young volunteers [...]

Essential hypertension is high blood pressure that has no obvious external cause. Left untreated, hypertension may result in kidney disease, arteriosclerosis, or other serious disorders. Epidemiological studies have shown that people with hypertension are more likely to have low intake of potassium. A diet low in potassium is also likely to be different from a high-potassium diet in many other ways. Therefore, it would invalid to assume that the low amounts of potassium contribute directly to the development of high blood pressure. To determine whether low potassium intake does, indeed, contribute directly to high blood pressure, 12 hypertensive, but otherwise healthy, subjects were given specially prepared meals in which only the potassium content was varied. The subjects ate standardized meals for five days, at which point they were switched to comparable meals low in potassium for the next 10 days. The sodium content of the meals was held constant throughout the experiment. At the end of 10 days, the blood pressure of the patients had increased. The average systolic (peak) blood pressure was 148 milliliters of mercury (mm Hg), in contrast with 141 mm Hg at the beginning of the low potassium diet. Similarly, the average diastolic blood pressure also rose to 96 mm Hg from 90 mm Hg. Blood and urine specimens taken during the course of the study indicated that the patients tended to retain sodium while on the low- potassium diet; at the same time, the excretion of calcium also rose. (A simultaneous increase in phosphorous excretion suggests that the calcium came from bone.) These changes may contribute to the elevation in blood pressure that occurs as body potassium is depleted. The details of the interactions between sodium, potassium, and calcium and their influence on blood pressure are not fully understood. (Consumer Summary produced by Reliance Medical Information, Inc.)

Diuretics are still among the most frequently used antihypertensive drugs in the treatment of hypertension. Their pharmacologic and hemodynamic properties are based on the water and salt metabolism in the pathophysiology of high blood pressure. Initially, there is a reduction of plasma and extra-cellular fluid volume; cardiac output also decreases. After this early phase, cardiac output returns to normal with an accompanying decrease in peripheral resistance so as to correct the underlying hemodynamic fault of the hypertensive state. Diuretics have a high therapeutic efficacy either as monotherapy or in combination with [Beta] blockers, angiotensinconverting enzyme inhibitors or calcium antagonists. The main problem with the use of diuretics is related to their metabolic side effects, which are dose-related. Currently, there is a tendency to administer low-dose diuretics, which result in fewer clinical and metabolic side effects, but with a continued antihypertensive efficacy. Therefore, low doses of diuretics can be recommended as initial therapy in the stepped-care approach of hypertension. (Am J Cardiol 1990;65:72H-76H), Diuretic drugs are the most frequently prescribed treatment for hypertension and are recommended for initial therapy by the World Health Organization. Since their use is not without some adverse effects, however, the mechanisms of action and biochemical effects of diuretics should be reviewed. Initially, diuretics work by reducing the volume of extracellular fluid, which decreases the cardiac output. The cardiac output slowly returns to normal, with a compensatory decrease in the resistance of the blood vessels to blood flow. This resistance is the primary determinant of hypertension, and its reduction is the basis for long-term management of hypertension. Although the mechanism by which diuretics maintain the state of low vascular resistance is not certain, they may directly reduce the reactivity of the vessels to constricting influences. There may also be a contribution from the reduction of sodium and calcium in the smooth muscle cells of the arteries. The moderation of sodium, or salt, intake may contribute to this effect. In addition, diuretics may assist the action of other antihypertensive drugs such as minoxidil or hydralazine, which dilate blood vessels but also promote sodium retention. Although diuretics promote the loss of potassium as well as sodium, this loss may be countered by the use of prescribing more moderate diuretic doses, or the use of potassium supplements. Side effects of diuretics include nausea, dizziness, rash, cramps, and impotence. Many of these may be controlled by the use of low-dose treatments. Biochemical abnormalities include glucose intolerance, which may lead to diabetes in some individuals, particularly those with a family history of diabetes. Increases in uric acid in the blood are observed, but are generally not regarded as worth treating unless levels exceed 65 micromolar in women or 77 in men. Increases in serum triglycerides and low-density lipoproteins are observed, and may negate some of the beneficial effects of blood pressure reduction. Indapamide, a indoline diuretic with a mechanism similar to the thiazides, seems to effectively reduce blood pressure without the concomitant effects on serum lipids. (Consumer Summary produced by Reliance Medical Information, Inc.)

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