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PubMed1986

Ouabain binding and inotropy in acute potassium depletion in guinea pigs.

In hypokalaemia the incidence of cardiac toxicity with digitalis is increased, possibly through changes in the affinity or capacity of the digitalis receptor in the heart. Previous studies have reported an increased ouabain binding capacity or Na+-K+ ATPase activity after hypokalaemia in human erythrocytes and rabbit and guinea pig hearts and no change or decreases in rabbit or rat skeletal muscles with no changes in ouabain affinity. The present study determined (a) the effect of potassium on 3H-ouabain binding to normokalaemic guinea pig cardiac cell membranes, (b) the effect of acute hypokalaemia induced by a potassium deficient diet for 14-18 days in guinea pigs on 3H-ouabain binding to erythrocytes and cardiac and skeletal muscle homogenates, and (c) ouabain induced inotropy in isolated contracting guinea pig left atria, right ventricular papillary muscles, and soleus muscle strips from normokalaemic and hypokalaemic guinea pigs. 3H-ouabain binds to cardiac cell membranes in the presence of magnesium and inorganic phosphate with an affinity (KD value) of 1.13 X 10(-7) mol X litre-1. Potassium decreased this affinity without changing the binding capacity. Erythrocytes and heart muscle homogenates showed the same affinity as cardiac cell membranes, whereas soleus muscle homogenates had a higher affinity for ouabain (KD 5.1 X 10(-8) mol X litre-1). After hypokalaemia, the ouabain affinity did not change in any tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Hypokalemia, cardiac failure, and reporting NXY-059 safety for acute stroke.

NXY-059, an alpha-phenyl-N-tert-butyl nitrone derivative, is a free radical-trapping agent presently in late clinical trials as a potential neuroprotectant limiting reperfusion injury following acute stroke. Two recent trials suggest that NXY-059 causes hypokalemia and associated cardiac disturbances. With regard to the mechanism of such association, most investigators agree that potent trapping of free radicals leads to the 11 beta-hydroxysteroid dehydrogenase blockade in kidneys, diminishing renal hydrocortisone oxidation and increasing K(+) ion urine excretion. Importantly, potassium deficiency represents the major avoidable cause of the array of serious cardiac adverse reactions: QT-prolongation, Torsades de pointes and other life-threatening arrhythmias, and higher risks for perioperative cardiopulmonary resuscitation and cardiac death. Because a prime target for NXY-059 use will likely be acute strokes in the emergency room environment, the potential combination of the drug with intensive therapy including fluid infusions, particularly with diuretics, might be especially harmful because of the synergic depletion of potassium, which might also jeopardize the fate of the novel nitrone neuroprotectant.

Adverse Drug Reaction Reporting Systems↗
PubMed2006

[Symptomatic periodic paralysis secondary to primary Sjogren's syndrome].

INTRODUCTION: Hypokalaemic periodic paralysis can be primitive or secondary to potassium deficiency which can arise from several causes. Primary Sjogren's syndrome is a rare cause related to kidney involvement. CASE REPORT: A 50-year-old woman has been admitted for hypotonic tetraparesis which had appeared a few days earlier. History taking revealed three previous similar episodes with a notion of oral and lacrimal dryness. Laboratory tests revealed severe hypokalaemia, hyperchloremia, alkaline urinary pH and a minima 24h proteinuria. Additional investigations led to the diagnosis of a primary Sjogren's syndrome defined on the basis of international criteria. Kidney biopsy revealed tubular-interstitial nephritis. Oral corticosteroïd therapy and potassium supplementation led to symptom improvement. A recurrent episode also responded to treatment. Additional urinary alkalinisation has prevented further relapse. DISCUSSION: Primary Sjogren's syndrome is an exocrine disease causing systemic disorders. Tubular-interstitial nephropathy may occur in 25 percent of patients leading to distal tubular acidosis defined by the association of hypokalaemia, hyperchloremia and alkaline urinary pH. When hypokalaemia is severe, periodic paralysis may occur. CONCLUSION: Primary Sjogren's syndrome can lead to nephropathy and subsequent hypokalaemic periodic paralysis. Urinary alkalinisation is essential to prevent this catastrophic presentation from recurring.

Adrenal Cortex Hormones↗
PubMed1981

Stimulation of aldosterone biosynthesis by experimental edema: role of the kidneys.

The role of the kidneys in the stimulation of aldosterone biosynthesis by sodium sequestration was investigated in potassium-depleted rats. After 2 wk on a potassium-deficient diet, rats were treated by subcutaneous injections of polyethylene glycol or formalin and were then kept on sucrose and water for 24 h. Either type of experimental edema markedly enhanced the conversions of tritiated deoxycorticosterone and corticosterone to aldosterone and 18-hydroxycorticosterone by incubated capsular portions of the adrenal glands and partially normalized the deranged pattern of endogenous corticosteroid output in response to serotonin. Bilateral nephrectomy completely blocked these effects of edema on the zona glomerulosa. When uremia was induced by bladder resection, with the kidneys left intact, edema still significantly stimulated aldosterone biosynthesis. Irrespective of increases in the plasma creatinine, the plasma potassium remained at uniformly low levels in all experimental groups of animals. According to these observations, experimental edema stimulates late steps of aldosterone biosynthesis in potassium-depleted rats by mediation of the kidneys, most likely through the renin-angiotensin system.

18-Hydroxycorticosterone↗
PubMed1976

Glucose tolerance and insulin release in malnourished rats.

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional immaturity' of the pancreas.

Aminophylline↗
PubMed2003

Regulated expression of Arabidopsis shaker K+ channel genes involved in K+ uptake and distribution in the plant.

Potassium is the most abundant cation in the cytosol, where it plays a role in basal functions. Rapid uptake and distribution of K+ is therefore required for plant growth. Three members of the so-called Shaker K+ channel gene family (nine genes identified in Arabidopsis) play a role in these transports: AKT1, SKOR and AKT2. The encoded proteins are involved in K+ uptake by the root, K+ secretion into the xylem sap and K+ transport in the phloem tissues, respectively. Using the GUS reporter strategy, we have found that another Shaker channel gene, AtKC1, is expressed in epidermal and cortical cells in roots (supporting the hypothesis of a role in K+ uptake from the soil, together with AKT1), and in trichomes and hydathodes in leaves. These four genes were selected for expression studies, and two-hybrid experiments were performed for channels displaying overlapping expression patterns. The data support the hypothesis that physical interactions could occur in planta between AtKC1 and AKT1, and between AKT1 and AKT2. Potassium deficiency, salt stress and hormonal treatments (ABA, BA, 2,4-D) were found to differentially affect channel mRNA levels, each channel displaying its own regulation pattern. The most prominent effects were (1) a strong induction of AtKC1 transcript accumulation in leaves (hydathodes, trichomes and leaf epidermis) in response to NaCl treatment, suggesting a key role of the protein in adaptation to saline conditions, and (2) a strong decrease in SKOR transcript levels by hormones, supporting the hypothesis that K+ secretion into the xylem sap is under tight hormonal control.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1983

Hypokalaemia stimulates prostacyclin synthesis in the rat.

1. To examine the hypothesis that the normalcy of blood pressure, despite an increase in circulating angiotensin II, and the blood pressor hyporesponsiveness to infusion of pressor agents which are associated with hypokalaemia, are due to overproduction of prostacyclin, the principal prostaglandin (PG) synthesized by the vascular endothelium, we studied the effect of experimental hypokalaemia on the urinary excretion of immunoreactive 6-keto-prostaglandin F1 alpha, a stable metabolite of prostacyclin, in the rat. 2. The animals were fed on a potassium-deficient diet for 9 days. Twenty-four hour urine samples were collected daily for measurement of urinary excretion of immunoreactive 6-keto-PGF1 alpha, PGE2 and 13,14-dihydro-15-keto-PGF2 alpha (PGFM). 3. Hypokalaemia caused significant increases of the three prostaglandins measured. 4. We conclude that hypokalaemia is a potent stimulus of both renal and vascular prostaglandins. The results suggest that an increase in prostacyclin synthesis in peripheral blood vessel walls may be responsible for the resistance of blood pressure to infusion of pressor substances as well as for the normalcy of blood pressure, despite the presence of high circulating angiotensin II concentrations, in conditions associated with hypokalaemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1975

Effects of bretylium and lidocaine on ventricular fibrillation in the isolated rabbit heart.

We studied the effects of bretylium tosylate and lidocaine on ventricular fibrillation in the isolated, perfused rabbit heart induced by perfusion with potassium-deficient solutions and by premature stimuli. The purpose of the study was to determine if the reported antifibrillatory effects of the drugs could be reproduced in the absence of an intact sympathetic nervous system. Lidocaine in the concentration of 5 mug/ml. prevented ventricular fibrillation induced by both methods while bretylium, in concentrations of 25 to 50 mug/ml. prevented neither type of filbrillation. These results indicate that the antifibrillatory effects of lidocaine can be attributed to drug-induced alterations in cellular electrophysiology, whereas those of bretylium are independent of such changes. Our study suggests that the reported antifibrillatory capability of bretylium is related to the drug's effects at sympathetic nerve terminals and thus is dependent upon an intact sympathetic nervous system.

Animals↗
PubMed1981

Mechanism of hyperreninemia in the potassium-depleted rat.

Although dietary potassium deficiency (KD) results in an increase in plasma renin activity (PRA), the mechanism of this effect has not been elucidated. In the present study, isolated kidneys from normal rats or from rats made KD by diet were perfused at constant pressure (120 mm Hg) with a Krebs-Ringer-Bicarbonate medium containing albumin. KD led to an increase in PRA (3.6 vs. 1.1 ng angiotensin I ml per h, P less than 0.01), which was associated with a decrease in macula densa (MD) fluid delivery as estimated by urine flow (70 vs. 166 microliters/min per g, P less than 0.005), and an increase in renal vascular resistance (RVR) as perfusion flow rate was decreased from 34 to 24 ml/min per g, P less than 0.005. The increase in PRA was independent of the MD because PRA could not be suppressed when macula densa delivery was increased by perfusing KD kidneys with hypooncotic albumin. Moreover, when kidneys were made nonfiltering by perfusing with hyperconcotic albumin, PRA remained increased in KD kidneys (8.1 vs. 3.5 ng angiotensin I ml per h, P less than 0.01) despite the absence of MD delivery. Because the increase in PRA in both filtering and nonfiltering KD kidneys was associated with an increase in RVR, filtering and nonfiltering kidneys were perfused with the vasodilator papaverine. Despite lower tissue K levels in KD kidneys (278 vs. 357 mu eq/g, P less than 0.01), RVR and PRA were normalized in both filtering and nonfiltering KD kidneys perfused with papaverine. In conclusion, PRA is increased in the KD isolated perfused kidney. This increase occurs independently of both the MD and of tissue K levels and is mediated by the renal vascular receptor.

Animals↗
PubMed1990

Potassium depletion increases luminal Na+/H+ exchange and basolateral Na+:CO3=:HCO3- cotransport in rat renal cortex.

Most HCO3- reabsorption in proximal tubules occurs via electroneutral Na+/H+ exchange in brush border membranes (BBMS) and electrogenic Na+:CO3=:HCO3- cotransport in basolateral membranes (BLMS). Since potassium depletion (KD) increases HCO3- reabsorption in proximal tubules, we evaluated these transport systems using BBM and BLM vesicles, respectively, from control (C) and KD rats. Feeding rats a potassium deficient diet for 3-4 wk resulted in lower plasma [K+] (2.94 mEq/liter, KD vs. 4.47 C), and higher arterial pH (7.51 KD vs. 7.39 C). KD rats gained less weight than C but had higher renal cortical weight. Influx of 1 mM 22Na+ at 5 s (pHo 7.5, pHi 6.0, 10% CO2, 90% N2) into BLM vesicles was 44% higher in the KD group compared to C with no difference in equilibrium uptake. The increment in Na+ influx in the KD group was DIDS sensitive, suggesting that Na+:CO3=:HCO3- cotransport accounted for the observed differences. Kinetic analysis of Na+ influx showed a Km of 8.2 mM in KD vs. 7.6 mM in C and Vmax of 278 nmol/min/mg protein in KD vs. 177 nmol/min/mg protein in C. Influx of 1 mM 22Na+ at 5 s (pHo 7.5, pHi 6.0) into BBM vesicles was 34% higher in the KD group compared to C with no difference in equilibrium uptake. The increment in Na+ influx in the KD group was amiloride sensitive, suggesting that Na+/H+ exchange was responsible for the observed differences. Kinetic analysis of Na+ influx showed a Km of 6.2 mM in KD vs. 7.1 mM in C and Vmax of 209 nmol/min/mg protein in KD vs. 144 nmol/min/mg protein in C. Uptakes of Na(+)-dependent [3H]glucose into BBM and [14C]succinate into BLM vesicles were not different in KD and C groups, suggesting that the Na+/H+ exchanger and Na+:CO3=:HCO3- cotransporter activities were specifically altered in KD. We conclude that adaptive increases in basolateral Na+:CO3=:HCO3- cotransport and luminal Na+H+ exchange are likely responsible for increased HCO3- reabsorption in proximal tubules of KD animals.

Animals↗
PubMed2000

Oligodendrocyte progenitor cells internalize ferritin via clathrin-dependent receptor mediated endocytosis.

We previously demonstrated ferritin binding is specific to white matter in mouse and human brain tissue and is not found within Multiple Sclerotic plaques. These results suggest that ferritin receptors are selectively expressed on oligodendrocytes. The present studies were designed to test the hypothesis that oligodendrocyte progenitor cells selectively bind ferritin and internalize it by methods consistent with receptor-mediated endocytosis. Using a cell culture system enriched for oligodendrocyte progenitor cells, we determined, that oligodendrocyte progenitor cells bind ferritin in a saturable and competitive manner with a K(d) of 5 nM and a receptor density of 0.06 fmol bound/20,000 cells. FITC tagged ferritin is internalized by A2B5, O4 or CNPase expressing cells in the culture, but not by GFAP+ cells. The uptake of ferritin into the oligodendrocyte progenitors was inhibited by treating the cells with inhibitors of receptor mediated endocytosis (hypertonic medium, potassium deficient medium, ATP depletion, sulfhydryl reagents). In addition exogenous ferritin decreased iron responsive element/iron regulatory protein binding indicating that the iron within the internalized ferritin is released and contributes to the intracellular iron pool. Given the relatively high amount of iron that can be delivered via ferritin, and the selective distribution of ferritin receptors in the white matter tracts in vivo, we propose that ferritin is a major source of iron for oligodendrocytes.

Animals↗
PubMed1981

Bicarbonate reabsorption in the papillary collecting duct of rats.

Using the technique of capillary perfusion and simultaneous luminal stop flow microperfusion the reabsorption of bicarbonate and glycodiazine from the papillary collecting duct was evaluated. Starting with equal H14CO3- and 3H-glycodiazine concentrations in the luminal and peritubular perfusates, the decrease in the luminal concentration at 10 and 45 s contact time was measured. In control rats with 25 mmol/l HCO3- in the perfusates the rate of HCO3- reabsorption calculated from the 10 s values was 0.34 nmol cm-2 s-1. In acute metabolic acidosis, the rate of bicarbonate reabsorption was 2,3 times higher. In metabolic alkalosis, the rate of bicarbonate absorption dropped to 13% of the control values. Also the 45 s values of acidotic and alkalotic animals differed significantly from each other. With 25 mmol/l glycodiazine in both perfusates the rate of buffer reabsorption as calculated from the 10 s values was 0.76 nmol cm-2 s-1 in control rats and did not deviate significantly from this value in acidotic and alkalotic animals. In control rats the bicarbonate reabsorption in % was the same, no matter whether both luminal and capillary perfusate contained 25 mmol/l bicarbonate or 10 mmol/l. In acidotic rats the rate of HCO3- reabsorption did not change significantly if all Na+ in the perfusates was replaced by choline (0.88 versus 0.79 nmol cm-2 s-1 at 25 mmol/l HCO3-). When in acidotic rats. 0.1 mmol/l acetazolamide or 1 mmol/l SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid) was added to both perfusates the rate of HCO3- reabsorption dropped by 75 and 58%, respectively. A potassium deficient diet for one week and DOCa administration had no influence on the bicarbonate reabsorption of rats which were on standard diet. The data indicate that (1) the buffer reabsorption from the papillary collecting duct is rather due to H+ ion secretion than to buffer anion reabsorption. (2) The adaptation to metabolic acidosis and alkalosis is specific for bicarbonate and not seen with glycodiazine. (3) Within the concentration range tested the HCO3- reabsorption rises linearly with the HCO3- concentration. (4) The HCO3- reabsorption in the papillary collecting duct is Na+-independent, it can be inhibited by acetazolamide and SITS, but is not influenced by K+-deficient diet plus DOCA.

Absorption↗
PubMed1994

Which diuretic to use?

The choice of a diuretic depends on knowledge of its efficacy in different disease states as well as the complications associated with its use. However, efficacy of the various diuretic agents as determined in healthy subjects may not always be applicable to the sick patient. The thiazide group appears to be the main offender with regard to hypokalemia and metabolic upsets; these complications seem to stem from long-term use and high dosages. Interest has been expressed on the influence of diuretic induced hypokalemia (and intracellular potassium deficiency) in inducing insulin resistance. The lipid abnormalities may arise as a result of this resistance or may be consequent on hyperinsulinemia from other as yet undetermined mechanisms. In addition, hypertension per se may be associated with insulin resistance. It is interesting to speculate that diuretics, which are commonly used in the treatment of hypertension, may, in some way, perhaps via the induction of hypokalemia, unmask this resistance.

Diuretics↗
PubMed2003

Prevention of cardiac arrhythmias in pediatric patients with normotensive-hypokalemic tubulopathy. Current attitude among European pediatricians.

Potassium deficiency predisposes to cardiac arrhythmias culminating in syncope or sudden death. Because of the uncertainty related to the possible occurrence of such cardiac arrhythmias in the context of normotensive-hypokalemic tubulopathies, 19 European pediatric nephrologists with a large experience of normotensive-hypokalemic tubulopathies were asked to answer a questionnaire. The responses suggest that inherited normotensive-hypokalemic tubulopathies per se do not strongly predispose to dangerous cardiac arrhythmias. However, cardiac arrhythmias may be acutely precipitated by drugs that prolong the QT interval, by diarrhea, or vomiting, and perhaps even by physical activity. Finally, the likelihood of dangerous arrhythmias in normotensive-hypokalemic tubulopathy is currently unknown.

Arrhythmias, Cardiac↗
PubMed1989

Purification and characterization of two distinct forms of rat adrenal cytochrome P450(11) beta: functional and structural aspects.

It is generally accepted that the last three steps of aldosterone biosynthesis are catalyzed by a single enzyme, i.e., cytochrome P450(11) beta (P450XIB). We have previously reported that rat adrenal mitochondria may be capable of producing two forms of P450(11) beta which differ in molecular weight (49 and 51 kDa). In the present study we describe the purification, the enzymatic activities, and some structural properties of these two proteins. Using zona fasciculata mitochondria, the 51-kDa protein was purified to electrophoretic homogeneity by means of octyl-Sepharose chromatography. In a reconstituted system the protein catalyzed 18- and 11 beta-hydroxylation of deoxycorticosterone, but exhibited no 18-hydroxylation or 18-hydroxydehydrogenation of corticosterone. The 49-kDa protein was isolated from zona glomerulosa mitochondria of rats kept on a low-sodium, high-potassium regimen. Using octyl-Sepharose chromatography, it could be separated from the 51-kDa protein. A reconstituted eluate fraction, containing the 49-kDa protein, converted deoxycorticosterone not only to 18-OH-deoxycorticosterone and corticosterone, but also to 18-OH-corticosterone and aldosterone. These findings indicate that the rat adrenal cortex is capable of producing two distinct forms of active cytochrome P450(11) beta. A structural relationship of the 49- and 51-kDa proteins was indicated by experiments involving limited proteolysis. Thus, digestion with alpha-chymotrypsin and V8-protease yielded very similar peptide maps for both proteins. During potassium repletion of potassium-deficient rats, the disappearance of the active 51-kDa protein coincided with the appearance of the 49-kDa protein. These results are suggestive of a post-translational processing mechanism converting the 51-kDa protein into the smaller 49-kDa form. However, the 49-kDa protein might also be encoded by a distinct gene, regulated separately depending on the physiological conditions.

Adrenal Cortex↗
PubMed1978

Severe hypercapnia associated with a non-respiratory alkalosis.

A case of hypoventilation in response to a non-respiratory alkalosis is presented. It is postulated that the degree of hypoventilation encountered was a normal response and that a fall in intracellular hydrogen ion concentration was responsible for the hypoventilation. This explains why the alkalosis associated with potassium deficiency is not associated with hypoventilation since the intracellular hydrogen ion concentration then remains constant. The renal response in this condition is responsible for maintaining the alkalosis and seems to be aimed at sodium conservation and hence plasma volume control rather than defence of acid-base balance.

Alkalosis↗