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PubMed1984

Potassium deficiency and cardiac function: experimental and clinical aspects.

Intra- and extracellular potassium and magnesium gradients in cellular membranes are essential factors of physiologic functions. Intestinal and renal loss of these ions cause predominantly a decrease in cellular potassium and magnesium by lowering the extra-cellular concentrations. In close connection with these changes, the permeability of cellular membranes for ions and, consequently, the excitability of skeletal and heart muscle cells are altered. Changes in the excitation, i.e. increased rising rate of the action potential and alterations of the refractory period, provoke cardiac arrhythmias. It is assumed that in contrast to chronic potassium deficiency the net changes which are caused by a reduction of extracellular potassium in acute deficiency states predispose to glycoside toxicity. These changes may therefore explain the clinical observation that acute hypokalemia is associated with a greater glycoside sensitivity than chronic potassium deficiency. Recent findings indicate that antikaliuretic substances can prevent the incidence of cardiac arrhythmias and may reduce glycoside sensitivity of the heart not only by antikaliuretic effects, but also by a possible direct action on the myocardium. Positive inotropic actions have also been reported. The meachanism of these effects is not yet sufficiently clarified. With regard to the broad clinical application of antikaliuretic diuretics (aldosterone antagonists, amiloride and triamterene), we studied their effects on myocardial membrane properties. Aldosterone antagonists led to a significant concentration-dependent prolongation of action potential duration and, correspondingly, to a lengthening of the refractory period. Action potential duration showed a significant increase under the influence of amiloride. A shortening of the refractory period induced by glycoside was antagonized by triamterene. Thus, the administration of antikaliuretic diuretics seems to be useful in the therapy of congestive heart failure also with respect to their extrarenal cardiac effects. Potassium and magnesium deficiency significantly alter cellular membrane functions, especially under pathologic conditions as far as ionic permeability and active ion transport are concerned. We assume that these findings may further explain the persistence of cardiac arrhythmias and increased glycoside sensitivity due to potassium deficiency even after restoring normal extracellular potassium concentrations. Therefore prolonged potassium and magnesium) substitution should be provided in these conditions in spite of normal extracellular potassium concentration.

Animals↗
PubMedDate not supplied

[The calcium metabolism of myocardial mitochondria and sarcoplasmic reticulum in experimental potassium deficiency (author's transl)].

Mechanical Parameters of the whole, Langendorff-perfused cat heart and of isolated right ventricular papillary muscles are depressed in chronic potassium deficiency. 45Ca binding of sarcoplasmic reticulum (SR) was found to be diminished and correlated with a reduced contractility of the perfused hearts. 45Ca uptake of sarcoplasmic reticulum isolated from potassium deficient hearts was also reduced. The mitrochondrial 45Ca binding and endogenous Ca concentration were increased and there was a positive correlation between these two parameters. The data suggest that a reduced SR Ca binding plays a role in the depression of myocardial contractility in chronic potassium deficiency. Increased mitochondrial 45Ca binding in the presence of reduced 45Ca binding and uptake of sarcoplasmic reticulum suggests the possibility that mitochondria are an additional myocardial calcium pool in chronic potassium deficiency.

Animals↗
PubMed1996

Regulation of Arabidopsis thaliana (L.) Heynh Arginine decarboxylase by potassium deficiency stress.

Arginine decarboxylase (ARGdc) is the first enzyme in one of the two pathways to putrescine in plants. ARGdc enzyme activity has been shown to be induced by many environmental factors, including potassium deficiency stress. We investigated the mechanism for induction of ARGdc activity during potassium deficiency stress in Arabidopsis thaliana (L.) Heynh. We show that A. thaliana responds to potassium deficiency stress by increasing ARGdc activity by up to 10-fold over unstressed plants with a corresponding increase in putrescine levels of up to 20-fold. Spermidine and spermine levels do not increase proportionately. Northern analysis showed no increase in ARGdc mRNA levels correlated with the increase in ARGdc enzyme activity. Western analysis revealed that there was no difference between ARGdc protein levels in stressed plants compared with controls. The increase in ARGdc enzyme activity due to potassium deficiency stress does not appear to involve changes in mRNA or protein abundance.

Arabidopsis↗
PubMed1981

Inhibition of rabbit renal prostaglandin E2 biosynthesis by chronic potassium deficiency.

To test the hypothesis that renal PGs may mediate the renal functional defect of potassium depletion, rabbits were placed on normal potassium and potassium-deficient diets for 7 weeks, and measurements were made of urinary PGE2 excretion; renal cortical, medullary, and papillary PGE2 content; and in vitro, de novo PGE2 biosynthesis. In the sixth week maximal urinary osmolality declined significantly, from 1118 +/- 44 mOsm/kg of H2O in controls to 666 +/- 25 in potassium-deficient animals, accompanied by a corresponding decrease in urinary excretion of potassium from 12.2 +/- 0.7 mEq/24 hr to 0.93 +/- 0.1 and in muscle potassium content from 39.0 +/- 1.0 mEq/100 gm to 22.3 +/- 1.9. By 3 weeks urinary excretion of PGE2 was significantly lower in hypokalemic animals than in controls. Renal cortical, medullary, and papillary PGE2 tissue content decreased significantly, from 0.061 +/- 0.01 microgram/gm to 0.022 +/- 0.005, 0.73 +/- 0.09 microgram/gm to 0.267 +/- 0.036, and 8.6 +/- 1.04 microgram/gm to 4.6 +/- 1.4, respectively. In vitro PGE2 biosynthesis by cortical, medullary, and papillary slices from normal animals was 0.102 +/- 0.01, 9.55 +/- 1.7, and 25.5 +/- 2.8 microgram/gm/30 min, whereas corresponding values from hypokalemic rabbits were 0.04 +/- 0.006, 3.9 +/- 0.747, and 14.0 +/- 1.25 microgram/gm/30 min, respectively. These results indicate that renal slices from hypokalemic rabbits synthesize much less PGE2 in vitro than do normal controls. The date do not support the hypothesis that enhanced PGE2 synthesis mediates the renal concentrating defect of chronic potassium deficiency but suggest that decreased renal PGE2 production may underlie the impairment in renal hemodynamics known to exist in this condition.

Animals↗
PubMed1984

Role of the renin-angiotensin system in the regulation of late steps in aldosterone biosynthesis by sodium intake of potassium-deficient rats.

The role of the renin-angiotensin system in the adaptation of late steps in aldosterone biosynthesis to sodium intake was studied in potassium-deficient rats. Capsular portions of adrenal glands were incubated with [3H]corticosterone and conversion to aldosterone and 18-hydroxycorticosterone was measured by double isotope dilution and multiple paper chromatography. Sodium loading of sodium- and potassium-depleted rats resulted in a rapid and extensive fall in PRA but only in a delayed and gradual suppression of aldosterone biosynthesis. Treatment with the converting enzyme inhibitor, captopril, did not affect aldosterone biosynthesis in rats with established sodium and potassium deficiency, but blocked the stimulation of the conversion of corticosterone to aldosterone and 18-hydroxycorticosterone by sodium restriction of potassium-depleted rats. Infusion of a high dose of angiotensin II into potassium-deficient rats stimulated aldosterone biosynthesis depending upon the concurrent sodium intake. Accordingly, the renin-angiotensin system plays an important but limited role in the control of late steps of aldosterone biosynthesis by sodium intake. Angiotensin II seems to be essential for the induction but not for the maintenance of a high activity of the enzyme(s) involved in the conversion of corticosterone to aldosterone during combined sodium and potassium restriction. The sensitivity of the zona glomerulosa to the long term stimulatory action of angiotensin II varies with the sodium intake and appears to be regulated by the plasma potassium concentration and unknown other mediators.

18-Hydroxycorticosterone↗
PubMed1998

Pleiotropic effects of potassium deficiency in a heterocystous, nitrogen-fixing cyanobacterium, Anabaena torulosa.

Omission of potassium from the growth medium caused multiple metabolic impairments and resulted in cessation of growth of the filamentous, heterocystous, nitrogen-fixing cyanobacterium Anabaena torulosa, during both diazotrophic and nitrogen-supplemented growth. Prominent defects observed during potassium deprivation were: (i) the loss of photosynthetic pigments, (ii) impairment of photosynthetic functions, (iii) reduced synthesis of dinitrogenase reductase (Fe-protein), (iv) inhibition of nitrogenase activity, and (v) specific qualitative modifications of protein synthesis leading to the repression of twelve polypeptides and synthesis and accumulation of nine novel polypeptides. The observed metabolic defects were reversible, and growth arrested under prolonged potassium deficiency was fully restored upon re-addition of potassium. Such pleiotropic effects of potassium deficiency demonstrate that apart from its well-known requirement for pH and turgor homeostasis, K+ plays other vital specific roles in cyanobacterial growth and metabolism.

Anabaena↗
PubMed1976

Increase in the (Na+ + K+)-ATPase activity in heart muscle after chronic treatment with digitoxin or potassium deficient diet.

In guinea pigs, administration of digitoxin (0.3 mg/kg s.c. for 7-24 days) causes an increase in activity of the (Na+ + K+)-ATPase of the heart. The plasma K+ level and the K+ content of the heart muscle of these animals remains unchanged and there is no significant alteration in the digitoxin toxicity compared to controls. In guinea pigs with potassium deficiency produced by a potassium deficient diet for 12 days, there is a related increase of the (Na+ + K+)-ATPase. The plasma K+ level of these animals is diminished while the K+ content in the heart muscle remains unchanged the toxicity of digitoxin is enhanced. In both test groups the increase in the (Na+ + K+)-ATPase activity is limited to enzymes from heart muscle, those from brain or kidney remaining unaffected. This increase in activity seems to be the result of an adaptive enzyme induction.

Adenosine Triphosphatases↗
PubMed2002

Influence of different neural systems on the secretion of sex hormones in potassium deficient mice.

The influence of different neural systems that modulate GnRH secretion by hypothalamic neurons was investigated in mice exposed to hypokalemic conditions, in which the pulsatile release of GnRH has been shown to be altered and associated with a significant decrease of plasma sex steroids. Our results demonstrate that the potentiation of the inhibitory pathways mediated by opiates and GABA may be implicated in the decrease of sex hormones secretion produced by hypokalemia since treatment with higher doses of naloxone or flumazenil are required to restore progesterone or testosterone levels in potassium deficient mice. The combination treatment of prazoxin and naloxone suggests that the inhibitory action of opiates take place through its action on noradrenergic neurons. It is also possible that the inhibition of GnRH release could be due to a decrease in the tonic stimulatory action of noradrenergic pathway implicated in the control of GnRH release. Our results also reveal that it is unlikely that the glutamatergic system may play any relevant direct role in the decrease of sex steroid secretion observed in potassium deficient mice. Finally, these results together with the normal pattern of estradiol levels found along the estrus cycle in potassium deficient mice indicate that factors different from estradiol and acting on neural systems implicated in the regulation of GnRH-secreting neurons participate in the generation of the preovulatory surge of GnRH.

Animals↗
PubMed1985

Relationship of phosphate-dependent glutaminase activity to ammonia excretion in potassium deficiency and acidosis.

Ammonia production and excretion are elevated in potassium depletion alkalosis, although normally they are reduced in alkalosis and elevated in acidosis. Studies were conducted with or without acute acid loading in normokalemic rats or rats made chronically hypokalemic with deoxycorticosterone acetate and a potassium-deficient diet to examine the role of phosphate-dependent glutaminase (PDG) in regulating ammonia excretion. Renal cortical PDG rose fourfold, and urinary ammonia excretion (UAE) doubled in potassium depletion compared to potassium-repleted controls. Following acid challenge PDG and urinary ammonia increased four- to sevenfold in both normokalemic and hypokalemic animals, but the rise in UAE did not correspond to the increase in PDG. Thus, PDG levels in acidotic normokalemic rats were one half those seen in potassium-depleted rats, but UAE in the acidotic rats was six times greater. These results could not be explained solely by changes in blood pH. The poor correlation between PDG and UAE also could not be explained by limited substrate availability, since blood glutamine levels were unaffected by potassium depletion. The disparity between UAE and PDG in potassium depletion was studied further during 9 days of potassium repletion of depleted rats. UAE was again increased by depletion but, after only 3 days of potassium repletion, UAE fell to levels found in normokalemic rats. The renal PDG activity, however, remained three times normal. Indeed, PDG remained significantly elevated even after 9 days of potassium replacement. Other enzymes involved in renal ammoniagenesis, including delta glutamyl transferase, glutamine transferase and omega deamidase, were assayed, and alterations in their activities could not account for the changes in UAE.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1970

Effect of Potassium Deficiency upon Translocation of C in Detached Blades of Sugarcane.

The translocation of radioactive photosynthate was studied in blades detached from plants which had been grown in nutrient solution with and without potassium. Basipetal translocation decreased in the blades of plants deprived of potassium, even when deficiency symptoms were not visible. In such slightly potassium-deficient leaves, translocation was decreased in the light but not in the dark. More severe potassium deficiency decreased translocation both in darkness and in light. Potassium deficiency decreased translocation at light intensities giving no difference in rate of photosynthesis between plus and minus potassium leaves and even at light intensities at which there was no net fixation of carbon dioxide. At all levels of deficiency, the relative decrease in translocation was greater than the relative decrease in photosynthesis. Translocation was affected at potassium deficiency levels which had no effect upon photosynthesis.Potassium deficiency decreased translocation relatively more than it decreased moisture content. There was a much better correlation between the decrease in potassium and translocation than between the decrease in moisture and translocation.An experiment with radioactive phosphorus indicated an upset in phosphorylation in the stems of potassium-deficient plants.

Journal Article↗
PubMed1981

Cell division in kidneys of rats fed a potassium-deficient diet.

Mitoses is stimulated in the kidneys of adult rats fed a potassium-deficient diet. A statistically significant increase in mitotic figures appears first in the collecting ducts of the inner strip of the outer medulla after two days on the K+ deficient diet (P less than 0.05). After six days, mitosis also increases in the collecting ducts in the outer stripe and in the inner medulla (P less than 0.01). After eight days there is a significant rise in mitotic activity in the cells of the proximal convoluted tubule (P less than 0.01). There is a questionable increase in mitosis found only on the fifth day in the distal convoluted tubule. In all other cell types there is no statistically significant increase in cell division over the normal low levels that are observed in the cells of the controls rats.

Animals↗