Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Potassium Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2001

Glycosphingolipids modulate renal phosphate transport in potassium deficiency.

BACKGROUND: Potassium (K) deficiency (KD) and/or hypokalemia have been associated with disturbances of phosphate metabolism. The purpose of the present study was to determine the cellular mechanisms that mediate the impairment of renal proximal tubular Na/Pi cotransport in a model of K deficiency in the rat. METHODS: K deficiency in the rat was achieved by feeding rats a K-deficient diet for seven days, which resulted in a marked decrease in serum and tissue K content. RESULTS: K deficiency resulted in a marked increase in urinary Pi excretion and a decrease in the V(max) of brush-border membrane (BBM) Na/Pi cotransport activity (1943 +/- 95 in control vs. 1184 +/- 99 pmol/5 sec/mg BBM protein in K deficiency, P < 0.02). Surprisingly, the decrease in Na/Pi cotransport activity was associated with increases in the abundance of type I (NaPi-1), and type II (NaPi-2) and type III (Glvr-1) Na/Pi protein. The decrease in Na/Pi transport was associated with significant alterations in BBM lipid composition, including increases in sphingomyelin, glucosylceramide, and ganglioside GM3 content and a decrease in BBM lipid fluidity. Inhibition of glucosylceramide synthesis resulted in increases in BBM Na/Pi cotransport activity in control and K-deficient rats. The resultant Na/Pi cotransport activity in K-deficient rats was the same as in control rats (1148 +/- 52 in control + PDMP vs. 1152 +/- 61 pmol/5 sec/mg BBM protein in K deficiency + PDMP). These changes in transport activity occurred independent of further changes in BBM NaPi-2 protein or renal cortical NaPi-2 mRNA abundance. CONCLUSION: K deficiency in the rat causes inhibition of renal Na/Pi cotransport activity by post-translational mechanisms that are mediated in part through alterations in glucosylceramide content and membrane lipid dynamics.

Animals↗
PubMed1975

Influence of glycosides on myocardial potassium and sodium concentration in acute and chronic potassium deficiency.

The analytical assay of intracellular potassium ([Ki]) and sodium ([Nai]) concentration of guinea pig papillary muscle measured in in vitro experiments shows that: 1) 5 X 10(-7) M g-strophanthin causes a decrease of [Ki] under control conditions, in acute as well as in chronic potassium deficiency, 2) a more marked glycoside effect is seen when the extracellular potassium concentration is reduced from 4.7 to 2mEq/1; this finding, therefore, is in good agreement with the observation that glucoside binding to its receptor at the cellular membrane is enhanced when potassium concentration is decreased, 3) whereas in chronic potassium deficiency normal [Ki] and [Nai] are maintained, acute potassium deficiency is accompanied by a loss of cellular K and gain of cellular Na. Under the influence of cardioactive glycosides, in chronic potassium depletion higher intracellular potassium and lower intracellular sodium concentrations are maintained than in acute potassium depletion. It is supposed tha t the net changes which are caused by a reduction of [Ke] in acute potassium deficiency in contrast to chronical potassium deficiency predispose to glycoside toxicity. These changes may therefore be the cause of the clinical observation that acute hypokalemia is associated with a greater glycoside sensitivity than chronic potassium deficiency.

Acute Disease↗
PubMed1977

Phosphorus metabolism in potassium-deficient rats.

Hypophosphatemia as a consequence of potassium deficiency has been reported sporadically. Most cases have been complicated by other factors which might lead to decreased serum phosphorus levels. Therefore, the serum phosphorus in this study was measured in Sprague-Dawley rats with nutritionally induced potassium deficiency. Severe potassium depletion was manifested by hypokalemia (2.4 mEq/liter versus 3.9 mEq/liter in controls) and decreased muscle potassium content. Statistically significant hypophosphatemia did not develop, although decreased muscle phosphorus content was observed. Therefore, hypophosphatemia is not a regular accompaniment of severe potassium deficiency in the rat.

Animals↗
PubMed1983

Role of vasopressin in support of blood pressure in potassium deficient rats.

Arginine vasopressin (AVP) has been found to contribute to the maintenance of blood pressure (BP) in the rat. Since potassium deficiency results in alterations in systemic hemodynamics, the role of AVP in the control of BP was studied after 14 to 21 days of dietary potassium deficiency. When potassium deficient and control rats were allowed free access to water, plasma osmolality (301.4 +/- 1 vs. 293.4 +/- 3 mOsm/kg; P less than 0.02) and plasma AVP (3.5 +/- 0.2 vs. 2.4 +/- 0.2 pg/ml; P less than 0.02) were increased in potassium deficient animals. To determine the role of this increase in AVP in the maintenance of BP, BP was determined in rats made polydipsic by adding glucose to the drinking water. In both control and potassium deficient rats, increased fluid intake resulted in increased urine output, decreased urinary and plasma osmolality, and a decrease in plasma AVP. While there was no change in BP in control rats when fluid intake was increased, BP fell from 103.9 +/- 1.8 to 96 +/- 2.6 mm Hg (P less than 0.05) in potassium deficient rats with increased fluid intake. To confirm that the decrease in plasma AVP caused the decrease in BP in potassium deficient rats, an AVP pressor antagonist was employed. Following the administration of the AVP pressor antagonist, there was no change in BP in control animals. In contrast, BP fell from 104.3 +/- 1.9 to 98.3 +/- 2.5 mm Hg; P less than 0.05 in potassium deficient rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Angiotensin II type 1 receptor blockade ameliorates tubulointerstitial injury induced by chronic potassium deficiency.

BACKGROUND: Chronic potassium (K+) deficiency, one of the well-known causes of renal tubulointerstitial injury, is associated with an alteration in vasoactive mediators including persistent generation of renal cortical angiotensin (Ang) II despite the suppression of plasma Ang II, and suppression of urinary nitrite/nitrate excretion. We tested the hypothesis that K+-deficiency-induced renal tubulointerstitial injury could be mediated by Ang II or a reduction in nitric oxide. METHODS: Rats were fed a K+-deficient diet (0.01% K+) alone, or with either losartan or l-arginine (L-Arg) in drinking water. Control rats were fed with a normal K+ diet (0.36% K+). At the end of 10 weeks, kidneys were excised and renal injury was evaluated. RESULTS: Serum K+ was similarly depressed in all three groups receiving the K+-deficient diet. Rats on the K+-deficient diet alone developed renal hypertrophy and tubulointerstitial fibrosis with an increase in tubular osteopontin expression, macrophage infiltration and type III collagen deposition. Administration of losartan significantly reduced renal hypertrophy and prevented tubulointerstitial injury in the cortex, although some medullary injury occurred. In contrast, administration of L-Arg did not attenuate tubulointerstitial injury in the cortex, despite a complete recovery of urinary nitrate excretion. Mild but significant improvement of tubular osteopontin expression and macrophage infiltration were observed in the medulla of L-Arg-treated hypokalemic rats. CONCLUSIONS: These results indicate that hypokalemic renal injury is mediated, at least in part, by Ang II via the Ang II type 1 receptor, with a lesser contribution mediated by a reduction in nitric oxide. Losartan may be beneficial in preventing hypokalemic tubulointerstitial injury.

Angiotensin Receptor Antagonists↗
PubMed1963

THE EFFECT OF POTASSIUM DEFICIENCY ON THE REABSORPTION OF PROTEIN IN THE RENAL TUBULE OF THE RAT.

Male Wistar rats were made potassium-deficient by feeding a diet low in potassium, while controls were pair-fed the same diet supplemented with potassium. Four weeks later 10 mg of T-1824 was injected into each rat. It was found that the characteristic granules which accumulate in the renal collecting tubule cells as a result of potassium deficiency were colored blue and that a diminished coloration of the convoluted tubule cells of the kidney was present. Quantitative measurements of the renal T-1824 content showed that it was decreased as a result of potassium deficiency. The daily rate of protein excretion was increased by the potassium deficiency. It is concluded that potassium deficiency decreases reabsorption of protein in the convoluted tubules of the kidney and that increased proteinuria thus results. Also, the granules which appear in renal collecting tubule cells as a result of potassium deficiency contain serum protein, which probably enters the cells from the tubular lumen.

Animals↗
PubMed1983

Natural history of potassium-deficiency myopathy in the dog: role of adrenocorticosteroid in rhabdomyolysis.

Potassium deficiency occurs in several conditions and is reported to cause muscle weakness and rhabdomyolysis. The mechanisms by which potassium deficiency cause muscle disease remain unknown, but the primary purpose of the present study was to determine whether abnormal muscle glycogen metabolism causes muscle weakness, as suggested by previous work. We monitored the natural history of potassium deficiency in two groups of dogs, one of which also received deoxycorticosterone acetate (DOCA), an agent commonly used in other studies to accelerate potassium loss. Group I dogs on potassium-free diet alone showed a 41% decrease in muscle potassium, no change in serum CO2, creatine kinase (CK), or muscle phosphorylase activity and only mild histopathologic abnormalities before death, after 198 +/- 42 days on the diet (mean +/- S.D.). In contrast, group II dogs on the same diet plus DOCA developed clinically similar severe weakness and died more rapidly than group I, 37 +/- 7 days (p less than 0.03). DOCA dogs showed a more rapid decrease in muscle potassium to the same level as group I, a 37% increase in serum CO2, an increase in serum CK to 1060 to 2775 IU/ml, a 23% decrease in muscle phosphorylase activity, and severe muscle histopathology, including rhabdomyolysis. Neither group showed any change in body weight, electromyogram (EMG), muscle glycogen concentration, glycogen synthetase activity, serum or muscle magnesium or phosphorus, or serum T3 or T4. In conclusion, dietary potassium deficiency in dogs causes severe weakness and death without causing rhabdomyolysis or abnormal muscle glycogen metabolism. Adding DOCA to the potassium-free diet creates a different model characterized by rapid clinical deterioration and rhabdomyolysis.

Animals↗
PubMed2005

Plant responses to potassium deficiencies: a role for potassium transport proteins.

The availability of potassium to the plant is highly variable, due to complex soil dynamics, which are strongly influenced by root-soil interactions. A low plant potassium status triggers expression of high affinity K+ transporters, up-regulates some K+ channels, and activates signalling cascades, some of which are similar to those involved in wounding and other stress responses. The molecules that signal low K+ status in plants include reactive oxygen species and phytohormones, such as auxin, ethylene and jasmonic acid. Apart from up-regulation of transport proteins and adjustment of metabolic processes, potassium deprivation triggers developmental responses in roots. All these acclimation strategies enable plants to survive and compete for nutrients in a dynamic environment with a variable availability of potassium.

Acclimatization↗
PubMed1961

Potassium deficiency in marmots during hibernation.

Semiquantitation of potassium deficiency in the renal papillae indicates that woodchucks (Marmota monax) are deficient in potassium annually during the time they subsist on stored fats. The deficiency begins prior to hibernation, progresses during hibernation, and, in males, continues during the immediate postemergence period.

Animals↗
PubMed1977

The hemodynamic effects of potassium deficiency in the dog.

Potassium deficiency for 3 weeks in dogs caused 374 +/- 38 mEq of sodium retention with increase in body weight, plasma volume, and inulin space. Cardiac output increased from 3.7 +/- 0.6 to 5 +/- 0.6 liters/min (P less than 0.02) and systemic vascular resistance decreased from 3,050 +/- 590 to 2,000 +/- 286 dynes/cm per sec2 (P less than 0.05). Plasma renin activity (PRA) increased from 0.4 +/- 0.1 to 17.2 +/- 0.9 ng/ml per hour (P less than 0.01) without change in plasma aldosterone. Angiotensin sensitivity decreased from a rise of 37 +/- 4 mm Hg in mean arterial pressure (MAP) to 10 ng/kg per min before potassium depletion to a rise of 10 +/- 2 mm Hg after hypokalemia. Urinary prostaglandin E (PGE) excretion increased from control values of 1,224 to 1,556 ng/day to 9,352 +/- 3,670 after 21 days of hypokalemia (P less than 0.01). Indomethacin, 150 mg a day for 3 days, decreased urinary PGE to control values as PRA decreased from 17.2 +/- 5.9 to 1.1 +/- .3 ng/ml per hour and angiotensin sensitivity was partially restored. These findings indicate that hypokalemia increased urinary PGE with extracellular fluid volume expansion, decreased sensitivity to angiotensin and increase in PRA.

Angiotensin II↗
PubMed1986

Effect of indomethacin on papillary solute concentration in the potassium-deficient rat.

Administration of indomethacin or meclofenamate to normal rats increases renal papillary solute concentration primarily by enhancing solute addition. A reduction in papillary solute concentration is characteristic of potassium deficiency. Of the multiple factors probably responsible for this reduction, several can be influenced by indomethacin or meclofenamate. The present study examined the effect of indomethacin on papillary solute concentration in the potassium-deficient rat. Indomethacin increased papillary solute concentration in normal but not potassium-deficient rats when studied in the conscious hydropenic state. Since indomethacin could increase papillary plasma flow in the potassium-deficient rat, potentially negating any enhancement of solute transport into the papilla, papillary plasma flow and papillary Cl concentration were determined in anesthetized surgically manipulated rats. Base-line papillary Cl concentrations were reduced in this setting. Indomethacin increased papillary plasma flow only in potassium-deficient rats but increased papillary Cl concentration equivalently in normal and potassium-deficient rats. The ability of indomethacin to increase papillary solute concentration in the potassium-deficient rat seemingly depends upon the experimental setting.

Animals↗
PubMed1982

Changes in cellular and subcellular composition during potassium deficiency.

1. A specific dietary deficiency of potassium in young rats reduced the potassium concentration in thigh muscle by 48%, and in heart and kidney by 18%, but did not significantly affect the concentration in liver or brain. Conversely the sodium concentration rose in liver, heart and thigh muscle, and thigh muscle also accumulated increased amounts of magnesium. Apart from an increase in the water content of many tissues, no consistent changes in the composition of major cell constituents were observed. 2. The loss of potassium and accumulation of sodium and magnesium occurred predominantly in the supernatant fraction of the cell. The supernatant of all tissues studied contained about 80% of the total cellular potassium and sodium, and the potassium was present entirely in the ionic form. 3. Potassium and magnesium are the two most abundant intracellular metals, but their deficiencies have very different effects on the cell. The relationship between them is more complex than the inverse relationship between potassium and sodium.

Animals↗
PubMed1983

Effect of a potassium-deficient diet on arterial blood pressure, plasma and tissue cations, and tissue norepinephrine in the hypertensive dog.

Chronic potassium deficiency in one-kidney one-clip hypertensive dogs significantly reduces blood pressure and plasma potassium, with a simultaneous increase in plasma renin activity. Tissue potassium concentration was decreased and tissue sodium concentration was increased in striated muscle and adrenal glands, which may suggest that the sodium-potassium pump was inhibited. In myocardium the sodium concentration was higher but the potassium concentration was not significantly lower than in control hypertensive dogs on normal diets. Arterial cation concentrations in the potassium-deficient group were not significantly different from those in the control group. Tissue norepinephrine concentration was higher in arteries from potassium-deficient animals, significantly so in the mesenteric and femoral arteries. The conclusion is that potassium deficiency may decrease blood pressure in the one-kidney one-clip hypertensive dogs by impairing the release of norepinephrine.

Animals↗
PubMed1952

Effect of potassium deficiency on carbon dioxide, cation, and phosphate content of muscle, with a note on the carbon dioxide content of human muscle.

Albino rats weighing 160 to 175 gm. were fed a complete synthetic diet containing 0.003 per cent potassium and 0.7 per cent sodium for 40 days. Controls were given the same diet plus adequate added potassium. 1. Data from analyses of serum and skeletal muscle showed (a) a fall in serum chloride concentration and an increase in serum carbon dioxide concentration and pH in the potassium-deficient rats; (b) increases of sodium, magnesium, and calcium and a decrease of potassium in the muscle of the potassium-deficient rats; (c) no change of muscle chloride or carbon dioxide concentrations in the potassium-deficient rats. (2) Application of the Wallace-Hastings calculations to these data revealed (a) intracellular pH of the skeletal muscle of the normal rat to be 6.98 +/- 0.08; (b) an increase in serum partial pressure of carbon dioxide (pCO(2)) in potassium deficiency, together with increases in concentrations of [H(2)CO(2)] and [HCO(3) (-)] per kg. extracellular water and [H(2)CO(3)] per kg. cell water; (c) a decrease in values for [CO(2)] and [HCO(3) (-)] per kg. intracellular water; (d) a fall of intracellular pH in potassium deficiency to 6.42 +/- 0.05. (3) Analyses of sacrospinalis muscle from five men undergoing operation for ruptured intervertebral disc showed a mean value of 9.46 +/- 1.31 mM carbon dioxide per kg. blood-free tissue. Some problems of interpretation of data are briefly discussed.

Animals↗