Academic literature on the topic 'Plasma potassium levels'

Rossi R, Savastano S, Tommaselli AP, Valentino R, Iaccarino V, Tauchmanova L, Luciano A, Gigante M, Lombardi G. Percutaneous computed tomography-guided ethanol injection in aldosteroneproducing adrenocortical adenoma. Eur J Endocrinol 1995;132:302–5. ISSN 0804–4643 The feasibility, safety and effectiveness of percutaneous computed tomography-guided ethanol injection (PEI-CT) was investigated in a patient affected by aldosterone-producing adenoma (APA). A 42-year-old male patient with typical features of hyperaldosteronism presented a solitary left adrenal adenoma measuring 2 cm, with a normal contralateral gland, evidenced by both CT scan and adrenal [75Se-19]-nor-cholesterol scintigraphy. After normalization of potassium plasma levels, 4 ml of sterile 95% ethanol with 0.5 ml of 80% iothalamate sodium was injected. The procedure was completed in about 30 min. No severe pain or local complication was noted. Five hours after PEI, a fourfold and a twofold increase in aldosterone and cortisol plasma levels were observed, respectively. After 11 days on a normal sodium and potassium diet, normal potassium plasma levels and reduced aldosterone plasms levels were present, with reappearance of an aldosterone postural response. Plasma renin activity and aldosterone plasma levels normalized I month later, with reappearance also of a plasma renin activity postural response and maintenance of normal potassium plasma levels even on a high sodium and normal potassium diet. The patient has remained hypertensive, although lower antihypertensive drug dosages have been employed. After 17 months, normal biochemical, hormonal and morphological findings were still present. Thus, we suggest PEI-CT as a further alternative approach to surgery in the management of carefully selected patients with APA. Riccardo Rossi, Chair of Endocrinology, "Federico II" University of Naples, via Sergio Pansini 5, 80131 Naples, Italy

1. Eight patients with essential hypertension were challenged with an infusion of 32 mmol of potassium chloride in saline before and after control of their blood pressure by the angiotensin converting-enzyme (ACE) inhibitor enalapril. 2. The potassium infusion was associated with similar increases in plasma aldosterone before and during enalapril treatment, although absolute aldosterone levels were lower after enalapril treatment despite higher plasma potassium levels. 3. The handling of the potassium load was altered by ACE inhibition. The area under the curve of a plot of the increase in plasma potassium above baseline against time was greater during enalapril treatment than during treatment with placebo. 4. These observations contrast with data obtained in the dog and demonstrate that in patients with essential hypertension stimulation of aldosterone secretion by potassium is not abolished by chronic suppression of plasma angiotensin II; and although plasma aldosterone remains at a lower level, the homoeostasis of plasma potassium is only mildly impaired.

To study the role of aldosterone in the short-term control of potassium excretion, rats were gavaged with a liquid diet containing 10-20% of their daily caloric and potassium intake, with a range of sodium intakes. Levels of (effective) aldosterone at the time of gavage were manipulated by administration of spironolactone, aldosterone, and adrenalectomy. Urinary sodium, potassium, and creatinine excretion were measured in conscious unrestrained rats for 2 h after the food load, and then blood was collected for measurement of plasma potassium, aldosterone, and renin activity. Potassium excretion was dependent on both dietary potassium and a minimum dietary sodium content. Potassium excretion was reduced by spironolactone and adrenalectomy and increased by acute aldosterone treatment in most dietary groups. These results strongly suggest that the ambient levels of aldosterone are important in determining potassium excretion following food ingestion. Plasma aldosterone was higher with the higher potassium and lower sodium content diets. Changes in plasma aldosterone, with variations in dietary potassium or sodium, suggest a role for aldosterone in subsequent potassium excretion.

There were two main objectives for this study. The first of these was to develop a research methodology with which both the affinity and efficacy of B-adrenoceptor agonists on protein degradation in skeletal muscle could be studied.

B2-Adrenoceptors were isolated from toad skeletal muscle and were characterised in radioligand binding experiments. The resultant affinity constants for 14 drugs were compared with values obtained from bovine Bradrenoceptors, and paired t-test analysis indicated that no significant difference existed between these two populations of B2-adrenoceptors. Thus, toad skeletal muscle B2-adrenoceptors provide a suitable model for screening B-ligand affinities, and values may be extrapolated to the corresponding receptors in cattle (target species).

Recombinant Escherichia coli expressing human B1,-and human B2-adrenoceptors were also characterised in radioligand binding experiments. The data obtained verified that each clone provided a source of homogeneous receptors, which displayed the ligand binding affinities appropriate for the respective receptor subtype. Thus, recombinant bacteria are a useful tool for screening the subtype-selectivity of ligands.

The bacterial clone expressing human B2-adrenoceptors displayed ligand binding affinities that were not significantly different to drug affinity determinations performed with bovine B2-adrenoceptors. Thus, the B2-strain is a useful model of the Bradrenoceptor expressed in the skeletal muscle of cattle. Additionally, recombinant B2-adrenoceptors exhibited differential binding behaviour for agonists and antagonists: all antagonists tested displayed monophasic displacement curves, whereas agonist molecules having molecular weight of less than 250 g/mol and an octanol/water partition coefficient (log P) less than zero, displayed biphasic binding behaviour. From these experiments, the cloned Escherichia coli cell lines were selected as the preferred source of B2-adrenoceptors for radioligand binding screens.

The B-adrenoceptor agonist efficacy assay selected for this study was the isolated perfused rat hemicorpus. In the first experiment, the rate of 3-methylhistidine (3-MH) release from perfused hemicorpora was examined: the 3 MH efflux rate of 0.227 ± 0.009 Amo1/30 g/3 hours corresponded to a protein degradation rate of 8.7 ± 0.3 %/day. While this value was comparable to other estimates reported in the literature, the HPLC analytical technique used to quantify 3-MH was at the lower limit of detection sensitivity. This author was not confident that the small changes in 3-MH release that may result from B-agonist treatment would be detected using this method. Hence, an alternative approach of measuring proteolysis as a function of other essential amino acids was examined. With this second method, reincorporation of amino acid markers into protein was prevented by the protein synthesis inhibitor, cycloheximide. In the presence of radiolabelled phenylalanine and leucine, the addition of 40 Amo1/1 cycloheximide to the perfusion medium was found to inhibit protein synthesis by 78 to 90%, without influencing the composition of the free amino acid pools within muscle. Furthermore, this radiolabel incorporation data (for rat hindlimbs perfused in the absence of cycloheximide) enabled the protein synthetic rate of the muscle to be estimated at between 2.0 and 3.06 %/day.

When proteolysis is measured as a function of the release of essential amino acids, the rate of myofibrillar protein breakdown is indistinguishable from non-myofibrillar breakdown. Thus, specific increases in myofibrillar degradation may potentially be undetected. However, the probability of detecting significant changes in degradation may be improved by co-analysing a total of eight essential and semi-essential amino acids. This approach was endorsed when the amino acid efflux rate from rat hemicorpora perfused in the presence and absence of cycloheximide were examined: logically, the blockade of protein synthesis would be expected to result in elevated rates of amino acid efflux. Indeed, the amino acid efflux rates from cycloheximide treated tissues were consistently, though not necessarily significantly, higher than the rates determined in cycloheximide-free tissues. However, when a paired t-test analysis was performed with all eight amino acids, the level of statistical significance improved dramatically.

The results from perfusion experiments indicated that all subsequent studies of protein degradation should be performed in the presence of 40/Imola cycloheximide; and the essential amino acids, valine, methionine, tryptophan, phenylalanine, isoleucine, lysine, leucine, and the semi-essential amino acid tyrosine should be used as co-indices of the rate of protein degradation.

When rat hemicorpora were perfused in the presence of 40 Amo1/1 cycloheximide, the mean ± SEM rate of potassium released from 30 grams of skeletal muscle was 740 ± 60 Amo1/3 hours. Likewise, the mean ± SEM rate of glucose consumed by 30 grams of skeletal muscle was 330 ± 20 Amo1/3 hours. HPLC analysis of muscle amino acids derived from both intact rats, and from hemicorpora which had been perfused for three hours, revealed that the intracellular free amino acid content of muscle was not significantly altered by the perfusion process. Thus, the rate of protein degradation in perfused muscle tissue was estimated directly from the rate of amino acid efflux for eight essential/semi-essential amino acids.

The second major objective of this study was to use the rat hemicorpus preparation to determine whether the B2-adrenoceptor agonist, clenbuterol, mediates its growth promoting effects on skeletal muscle through a reduction in the rate of myofibrillar protein degradation.

Clenbuterol treatment (4 mg/kg diet, 265 μg/kg BWT/day) resulted in net protein accretion, and significantly enhanced the growth rate of treated animals. In mature male rats, clenbuterol treatment in the diet increased the rate of weight gain to 260% of the untreated level. However, the magnitude of the growth response declined after six days of treatment, which is consistent with B-adrenoceptor desensitisation. Clenbuterol-induced changes in blood flow to different tissues was evident from the change in the colour of adipose tissue in abdominal fat depots.

Clenbuterol treatment had no significant effect on either the perfusate pressure range or the rate of glucose uptake in perfused rat hemicorpora. In contrast, potassium efflux rates in chronically treated hindlimb preparations were elevated by 95%. The increase in potassium efflux may have been an artefact of the cycloheximide-induced inhibition of protein synthesis. However, more recent evidence of elevated plasma potassium levels in cows chronically treated with clenbuterol indicate that this may be a real effect of long-term B-agonist treatment.

When the rate of protein degradation was evaluated in terms of the sum of essential amino acids effluxed from perfused rat hemicorpora, acute (three hours) clenbuterol treatment caused a significant, but transient increase in proteolysis (11%). In contrast, longer-term clenbuterol treatment (6 and 12 days) effected a non-significant decrease in the rate of protein degradation (11.8 and 7.6%, respectively), and this effect was diminished over time, in a manner consistent with B-adrenoceptor desensitisation. Furthermore, the withdrawal of clenbuterol from chronically-treated tissues resulted in an immediate and significant increase (25.1%) in the rate of protein degradation, which indicates that the continued presence of clenbuterol is required to maintain the effect of reduced proteolysis.

Clearly, the reduction in the rate of protein degradation observed with chronic clenbuterol treatment is insufficient to account for the 160% increase seen in the growth rate of treated rats. Consequently, it can be concluded that protein synthetic rates must have also been elevated. Indeed, it has been estimated that the 160% increase in the growth rate of clenbuterol-treated rats could be accounted for by a net 16.4% change in the component processes of protein turnover (ie an 11.8% reduction in protein breakdown, and a 4.6% increase in protein synthesis). This is equivalent to a 10.25% change in protein turnover for every 100% increase in growth rate, and compares exceptionally well with the 10 to 13% change estimated by Kim and Sainz (1992).

From these studies, it was concluded that the mechanism of clenbuterol-induced muscle accretion includes components of both increased protein synthesis and decreased protein degradation. In tropical cattle, this saving in metabolic energy resulting from decreased proteolysis may offer an advantage to the animal during the dry winter months where seasonal weight losses are often observed.

Potassium is the major intracellular cation, and maintenance of potassium homeostasis is critical for normal cellular function. Serum potassium levels usually range from 3.5–4.5 mmol/l (compared with intracellular levels of ~150 mmol/l). Hypokalaemia is defined as a serum potassium level <3.5 mmol/l, and hyperkalaemia as a serum potassium level >4.5 mmol/l. Hyperkalaemia occurs in over 5% of hospitalized patients, and is most common in older age groups, where it is associated with renal impairment and medication use. Medications that block the renin–angiotensin system, such as angiotensin-converting-enzyme inhibitors and angiotensin receptor blockers, are often responsible. Hypokalaemia is also common, affecting over 15% of hospitalized patients, and is usually related to diuretic use, gastrointestinal losses, or inadequate potassium in the diet. This chapter reviews the causes and management of derangements of plasma potassium.

Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

Rhabdomyolysis is a potentially life-threatening syndrome characterized by the breakdown of skeletal muscle. It is associated with myalgia, muscle tenderness, swelling, and/or stiffness, accompanied by weakness and raised levels of creatine kinase (CK), myoglobin, phosphate and potassium, sometimes with acute kidney injury (AKI). There are multiple causes of this syndrome, traumatisms and myotoxic effect of drugs being the most frequent in developed countries. The pathophysiology involves direct trauma, as well as energy (ATP) depletion with disruption of sarcolemma integrity and muscle destruction. The sequestration of plasma water leads to hypovolaemic shock, while the release of muscle content, mainly myoglobin and potassium lead to the most severe complications of this syndrome, acute kidney injury/hyperkalaemia. The kidney injury is driven both by renal ischaemia due to vasoconstriction and to the toxic effects of myoglobin. The local oedema produced by the release of muscle content remains trapped within the fascia and can lead to compartment syndrome. Volume repletion with saline is essential to avoid hypovolaemic shock and acute kidney injury (AKI). With respect to compartment syndrome, close monitoring of clinical signs and compartment pressures is essential, since it can evolve to a surgical emergency. The prognosis of rhabdomyolysis is determined by age, baseline conditions and, most importantly, whether or not severe AKI develops.

Mineralocorticoid hypertension is characterized by increased distal renal tubular sodium reabsorption, raised body sodium content, plasma volume expansion, markedly reduced body potassium content, with a metabolic alkalosis and suppression of renin production by the juxtaglomerular cells of the kidney (and correspondingly low levels of angiotensin II). Primary aldosteronism is the most common cause of mineralocorticoid hypertension (1); less frequent causes include the rare inborn errors of adrenal steroid synthesis (11β‎-hydroxylase and 17α‎-hydroxylase deficiency), alterations in corticosteroid metabolism (syndrome of apparent mineralocorticoid excess), and constitutive activation of the epithelial sodium channel (Liddle’s syndrome).

Tubular function is critical for the maintenance of electrolyte and acid–base balance. Consequently, acid–base disorders typically manifest with alterations in plasma electrolyte concentrations and/or pH. Tubular handling of the various electrolytes is often linked on a molecular level. For example, secretion of potassium and protons in the collecting duct is dependent on sodium reabsorption. Consequently, tubular disorders typically present with characteristic patterns of electrolyte and acid–base abnormalities, which can serve as biochemical ‘fingerprints’ for the accurate diagnosis of the underlying disorder. Recognition of these ‘fingerprints’ is critical as correct identification of the underlying disorder is key for appropriate treatment.

Kidney is one of the tissues affected by age that involves cellular and structural changes inside the kidney and notably implicates with comorbidity, related to cardiovascular disease aging. Aging kidney causes the elderly susceptible to clinical deterioration from ordinary stimulation that younger individual can compensate, including acute renal injury, volume depletion or overload, sodium and potassium level disorders, and toxic reaction against kidney excreted drugs. As one of the organs with the fastest aging rate, kidney shows several age-related decline in both structural and functional with 30% of the glomerulus are damaged and represent diffuse glomerular sclerosis by age 75 and explain why the prevalence of chronic kidney disease (CKD) and end-stage renal disease are very common in the elderly. The cross-sectional population-based study by The National Health and Nutrition Examination Survey supports the theory of age-related decline in kidney function, although some other subjects did not have an absolute decline in kidney function. The underlying molecular mechanisms could be the target of future therapeutic strategies. Aging is a natural biological process characterized by a gradual decline in cellular function as well as progressive structural change of organ systems. In aging kidney, there are interactions of genetic factors, environmental changes, and cellular dysfunction that lead to the typical structural and functional changes. One of the most popular theory of aging is the theory of free radicals or oxidative stress based on the fact that cells are under chronic oxidative stress due to an imbalance between pro oxidants and antioxidants. Reactive oxygen species are oxygen-derived oxidizing compounds that are highly reactive, consisting of free radicals and non-radicals. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) refer to both reactive radicals and non-radical derivatives of oxygen and nitrogen. Reactive oxygen and nitrogen species (RONS) are produced by all aerobic cells and play an important role in aging as well as age-related diseases. Lipid peroxidation is a process of oxidative degradation of lipids that process by which free radicals bind to lipid electrons in the cell membrane resulting in direct cell damage. Lipid peroxidation can cause cellular damage in several ways such as impairing the integrity of the plasma membrane and subcellular organelles by peroxidation, “chain reaction” of ROS production, and activation of phospholipase A2 (PLA2) caused by lipid peroxidation. Fatty acids and other PLA2 metabolites (such as lysophospholipids) are known to damage cell membranes. In the development of kidney damage, the process of lipid peroxidation plays an important role. This is presumably due to the large number of long-chain polyunsaturated fatty acids (PUFAs) in the lipid composition of the kidneys and there are substantial evidence to suggest that ROS is involved in the ischemic, toxic, and immunologically mediated pathogenesis of renal injury, but the cellular mechanisms that result in cell injury and death are still being studied.

Assessment of plasma vWF abnormalities by clinical coagulation laboratories is difficult because the available test systems for vWF antigen quantification and multimer analysis are expensive, laborious, and require days, radioactive anti-vWF antibodies and autoradiographic methods. We have devised simple, rapid, sensitive alternative techniques for vWF quantification and multimer analysis that can be readily installed in clinical laboratories. Plasma vWF antigen quantification is by a 2 hour enzyme immunoassay that accurately detects levels as low as 0.23% of normal. Plasma vWF to be quantified is bound to polyclonal monospecific antihuman vWF attached to small glass beads, and anti-human vWF conjugated with alkaline phosphatase is added to make an insoluble "sandwich." A substrate solution consisting of phenylphosphate and 4-amino-antipurine is added, followed by potassium ferricyanide. Optical density (at 490-510 nm) of the red color that develops is directly proportional to the plasma concentration of vWF antigen. Plasma vWF multimeric analysis is by a one-day electrophoretic immunobiot procedure. Plasma vWF multimer forms are solubilized in SDS-urea-Tris-EDTA, separated by horizontal 1% agarose gel electrophoresis, and transferred to a cationic membrane. Other protein binding sites on the membrane are blocked with milk proteins, and the membrane is overlaid with anti-vWF IgG linked to alkaline phosphatase. vWF multimers are then displayed as blue bands by soaking the membrane in an alkaline solution of the histochemical stain, fast blue RR (commonly used for leukocyte alkaline phosphatase scoring) dissolved in naphtol AS-MX phosphate. These simple, non-radioactive procedures performed together permit the rapid distinction of classical (Type I) von Willebrand's disease (vWD), characterized by low vWF antigen and normal multimers, from the Type II vWD syndromes, characterized by a relative deficiency of the largest plasma vWF forms. Unusually large vWF multimers, present in remission plasma of patients with chronic relapsing thrombotic thrombocytopenic purpura (TTP), are also easily detected using this rapid system of multimer analysis.

The relevance of the research is due to the need to develop technologies for phytoremediation of the devastated lands in the mining and metallurgical regions of Ukraine and the world. In this regard, the creation of tree plantations adapted to the ecological conditions of such territories is considered by many experts as the most promising option for innovative technologies. However, the development of artificial woodlands requires knowledge of the pedogeochemical character- istics of devastated lands. The aim of the work was to carry out a comparative analysis of the macronutrients and heavy metals gross forms content in the soils of the devastated lands of the Kryvyi Rih mining and metallurgical region. The field studies focused on five contrasting monitoring sites of the Petrovsky dump (Central Kryvorizhzhya), which has a typical age and composition of rocks for the region. Soil sampling, drying, sieving, and sample preparation (sintering in a muffle furnace) were done in accordance with classical techniques. The concentrations of macronutrients (potassium, sodium, calcium, magnesium, sulfur, and phosphorus) and heavy metals (iron, manganese, zinc, copper, lead, and cadmium) were determined using an Inductively Coupled Plasma Mass Spectrometry (ICP- MS) X-Series 2 (Thermo Fisher Scientific, USA). The analytical part of our research was carried out on the basis of the laboratory of the Institute of Biosciences, Freiberg University of Technology and Mining Academy (Freiberg, Germany). At monitoring sites, significant differences were found in the content of macronutrients gross forms, and their variation relative to the control values as well. Potassium and sodium concentrations generally differed slightly or were close to control levels. The results of determining the content of calcium, magnesium and phosphorus indicate a significant deficiency or excess of these macronutrients in the soils of the devastated lands. An increased sulfur content was found in the soils of all monitoring sites, in some cases 4 times higher than the control level. The measured content of gross forms of iron, manganese, copper, cadmium and, partially, zinc in the soils of different monitoring sites exceeded the control values by 5.5 – 5.9 times. Thus, the analysis of the research results made it possible to establish that the soils of the devastated lands of the Petrovsky dump are characterized by unfavorable properties for the growth of most species of woody plants.