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PubMed1989

Physiology of magnesium metabolism and the important role of magnesium in potassium deficiency.

Magnesium, the second most abundant intracellular cation, has several critically important roles in the body. In addition to energy production and maintaining electrolyte balance, magnesium is essential for normal neuromuscular function as well as calcium and potassium transport. Evidence suggests that a deficit of magnesium is closely interrelated to potassium deficiency and refractory potassium repletion. Although the consequences of hypokalemia are widely documented and recognized, it is only recently that the importance of magnesium deficiency as a cause of potassium depletion has gained clinical attention. Because of the association between hypokalemia and ventricular ectopy/sudden death, familiarity with the causes of magnesium loss, as well as enhanced identification and treatment, appear to be important.

Hormones↗
PubMed1989

Effects of potassium deficiency on growth and protein synthesis in skeletal muscle and the heart of rats.

The effects of potassium deficiency on growth, K content and protein synthesis have been compared in 4-13-week-old rats. When maintained on K-deficient fodder (1 mmol/kg) rats ceased to grow within a few days, and the incorporation of [3H]leucine into skeletal muscle protein in vivo was reduced by 28-38%. Pair-feeding experiments showed that this inhibition was not due to reduced energy intake. Following 14 d on K-deficient fodder, there was a further reduction (39-56%) in the incorporation of [3H]leucine into skeletal muscle protein, whereas the incorporation into plasma, heart and liver proteins was not affected. The accumulation of the non-metabolized amino acid alpha-aminoisobutyric acid in the heart and skeletal muscles was not reduced. The inhibitory effect of K deficiency on 3H-labelling of muscle protein was seen following intraperitoneal (10-240 min) as well as intravenous (10 min) injection of [3H]leucine. In addition, the incorporation of [3H]phenylalanine into skeletal muscle protein was reduced in K-depleted animals. Following acute K repletion in vivo leading to complete normalization of muscle K content, the incorporation of [3H]leucine into muscle protein showed no increase within 2 h, but reached 76 and 104% of the control level within 24 and 72 h respectively. This was associated with a rapid initial weight gain, but normal body-weight was not reached until after 7 weeks of K repletion. Following 7 d on K-deficient fodder the inhibition of growth and protein synthesis was closely correlated with the K content of the fodder (1-40 mmol/kg) and significant already at modest reductions in muscle K content. In vitro experiments with soleus muscle showed a linear relationship between the incorporation of [3H]leucine into muscle protein and K content, but the sensitivity to cellular K deficiency induced in vitro was much less pronounced than that induced in vivo. Thus, in soleus and extensor digitorum longus (EDL) muscles prepared from K-deficient rats, the incorporation of [3H]leucine was reduced by 30 and 47% respectively. This defect was completely restored by 24 h K repletion in vivo. It is concluded that in the intact organism protein synthesis and growth are very sensitive to dietary K deficiency and that this can only partly be accounted for by the reduction in cellular K content per se. The observations emphasize the need for adequate K supplies to ensure optimum utilization of food elements for protein synthesis and growth.

Animals↗
PubMed1986

[Differential block of peripheral nerve fibers: the effect of lidocaine and potassium deficiency].

The combined effects of lidocaine and lack of glucose and potassium on conduction in A and C axons were investigated in vitro in rabbit vagus nerve. Extinction times of compound action potentials of A and C axons were determined in glucose and potassium deficient medium in the absence (group I, n = 6) or presence (group III, n = 6) of 0.1 mmol/l lidocaine hydrochloride. In group I, A fibers lost excitability within 120 +/- 9 min (mean +/- SEM) and the C axons within 133 +/- 6 min. In group III lidocaine prolonged significantly extinction times of both A and C axons (p less than 0.001); however, the conduction ceased in the unmyelinated (C) axons about 120 min later than in the myelinated (A) ones (p less than 0.05). In group II (n = 6) nerves were exposed to lidocaine for the same length of time as group I; these nerves exhibited an amplitude depression of the A and C potentials of less than 50%. In group IV, where 2 or 4 mmol/l KCl was present (n = 6 with each concentration) but no lidocaine, the extinction times decreased; the decrease was statistically significant for C axons but not for A axons. The analysis of nerve core electrolytes at the end of the exposures revealed the highest sodium and the lowest potassium contents in group III nerves. The controls (group I) contained more sodium and potassium than the nerves of group II. Thus a low concentration of lidocaine prolonged excitability in A and C axons deprived of glucose (group III).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1984

Influence of magnesium and potassium deficiency on renal elimination and cardiovascular function demonstrated by impedance cardiography.

In an open controlled trial with 6 male human volunteers Mg and K intake was reduced to 32-35% of normal during a 5- and 4-day period, respectively and 80 mg Furosemide/day was coadministered during the second period in order to induce Mg and K wasting. After each testing period an intravenous infusion of 27.87 mEq Mg and K was administered as K, Mg-D,L-aspartate during 2 h. Electrolyte and fluid balance were analysed before, during and after the testing period. Moreover, impedance cardiographic measurements were carried out in order to determine changes of cardiovascular function, and 24-hour ECGs were recorded simultaneously. It could be shown that reduced Mg and K intake induces depletion of the intracellular stores which was furthermore enhanced by coadministration of the loop diuretic Furosemide. Whereas Mg renal elimination amounted only to 60-54% of intake, K elimination exceeded intake to a considerable extent, a fact that could be explained by the lack of Mg. Changes of cardiovascular function, such as stroke volume, cardiac output and end-diastolic volume, expressed by alterations of total resistivity ZO, were less pronounced, but could be inverted at least partly by a single intravenous infusion of K,Mg-D,L-aspartate. Heart rate and 24-h ECG did not reveal any detectable change. The testing procedure described here can be considered a reliable model for tests in clinical pharmacology.

Blood Pressure↗
PubMed1973

Skeletal muscle resting membrane potential in potassium deficiency.

The resting transmembrane potential of skeletal muscle (E(m)) is thought to be a function of the ratio of intracellular to extracellular potassium concentration ([K(i)]/[K(o)]). In potassium deficiency, the fall of [K(i)] is proportionately less than the fall of [K(o)], thus theoretically predicting a rise of E(m). To examine this theory and to characterize E(m) in kaliopenic myopathy, muscle composition and E(m) were measured during moderate (n = 5) and severe (n = 11) K deficiency in the dog and compared with measurements in the severely K-deficient rat (n = 10). Mean measured E(m) rose during moderate K deficiency in four of five dogs (-85.4 to -94.6 mV) and during severe K deficiency in the rat (-89.1 to -94.9 mV). Both values closely approximated the increase in E(m) predicted by the Goldman equation. In contrast, during severe K deficiency in the dog, a significant decline (P < 0.001) of mean E(m) to -55 mV was observed.Since skeletal myopathy and paralysis do not occur in the rat as a consequence of K deficiency, the observation that E(m) falls as paralysis occurs in the unexercised dog suggests that alteration of muscle membrane function may play a role in kaliopenic myopathy. Such an event could explain the ease with which frank muscle necrosis may be induced by exercise in the K-deficient dog.

Acid-Base Equilibrium↗
PubMed1987

Prevalence of magnesium and potassium deficiencies in the elderly.

Concentrations of magnesium and potassium in erythrocytes and plasma were determined in a population of 381 unselected elderly men and women, most of them in their eighties. The effects of biological factors (age, sex, weight) and a large set of pathological conditions, malignant or not, were examined. Analyses of variance showed a relation between age and concentrations of plasma potassium and between weight and concentrations of plasma magnesium. The chi-square test showed correlations between low concentrations of plasma magnesium and diabetes, abuse of alcohol and tobacco, and also between low values for erythrocyte magnesium and hypertension. Low values for plasma potassium were correlated with hypertension whereas high values were correlated with cardiovascular disease. Although some of the differences in the mean concentrations observed were statistically significant, these differences were always small. Most interesting was the distribution of the concentrations of the cations. This study shows that assays of both of these cations in erythrocytes were better than assays in plasma to evidence a deficiency. Indeed, about 20% of the studied population had low concentrations of both erythrocyte potassium and magnesium, whereas 2 and 10% had low values for plasma potassium and magnesium, respectively. This study underlines the large prevalence of magnesium and potassium deficiencies in the elderly, an observation we could not attribute to pathology or treatment. Routine electrolyte studies therefore appear to be justified in aged human subjects.

Age Factors↗
PubMed1985

Current approaches to management of potassium deficiency.

Current issues related to oral potassium supplementation are reviewed, with emphasis on recommendations for the appropriate use of potassium supplementation for both replacement and preventive therapy. Dietary potassium intake, potassium-sparing diuretics, and the various forms of oral potassium supplements are reviewed in terms of indications for use, advantages, and limitations. Attention is given to controversial areas, i.e., gastrointestinal tolerance of controlled-release potassium oral dosage preparations and the need for potassium supplementation in hypertensive patients treated with diuretics.

Administration, Oral↗
PubMed1970

Effects of chronic potassium deficiency on plasma renin activity.

Serial determinations of plasma renin activity, sodium balance, urinary potassium excretion rate, and plasma sodium and potassium concentration were done in five dogs during dietary-induced potassium depletion and repletion. Duration of depletion for the different animals ranged from 5 to 7 wk. Plasma renin activity increased in all animals during depletion, with rises being demonstrated as early as the 1st depletion day in two of the dogs. Maximum values in the five dogs were recorded from the 2nd to the 28th day of depletion. Early in depletion, changes in renin activity did not correlate with changes in sodium balance. Late in the course of depletion, plasma renin activity decreased concurrently with a progressive retention of sodium. However, in every case increased renin activity persisted throughout depletion despite development of sodium retention sufficient to inhibit renin release in normal dogs. Potassium repletion resulted in a prompt decrease in renin activity to predepletion values. This study indicates that potassium deficiency has a stimulatory effect on renin release that is independent of any effect on sodium balance.

Animals↗