Potassium Depletion Research Articles

Cloning of a high-affinity K+ transporter gene PutHKT2;1 from Puccinellia tenuiflora and its functional comparison with OsHKT2;1 from rice in yeast and Arabidopsis

A high-affinity K+ transporter PutHKT2;1 cDNA was isolated from the salt-tolerant plant Puccinellia tenuiflora. Expression of PutHKT2;1 was induced by both 300 mM NaCl and K+-starvation stress in roots, but only slightly regulated by those stresses in shoots. PutHKT2;1 transcript levels in 300 mM NaCl were doubled by the depletion of potassium. Yeast transformed with PutHKT2;1, like those transformed with PhaHKT2;1 from salt-tolerant reed plants (Phragmites australis), (i) were able to take up K+ in low K+ concentration medium or in the presence of NaCl, and (ii) were permeable to Na+. This suggests that PutHKT2;1 has a high affinity K+-Na+ symport function in yeast. Arabidopsis over-expressing PutHKT2;1 showed increased sensitivities to Na+, K+, and Li+, while Arabidopsis over-expressing OsHKT2;1 from rice (Oryza sativa) showed increased sensitivity only to Na+. In contrast to OsHKT2;1, which functions in Na+-uptake at low external K+ concentrations, PutHKT2;1 functions in Na+-uptake at higher external K+ concentrations. These results show that the modes of action of PutHKT2;1 in transgenic yeast and Arabidopsis differ from the mode of action of the closely related OsHKT2;1 transporter.

Potassium restriction, high protein intake, and metabolic acidosis increase expression of the glutamine transporter SNAT3 (Slc38a3) in mouse kidney

Kidneys produce ammonium to buffer and excrete acids through metabolism of glutamine. Expression of the glutamine transporter Slc38a3 (SNAT3) increases in kidney during metabolic acidosis (MA), suggesting a role during ammoniagenesis. Potassium depletion and high dietary protein intake are known to elevate renal ammonium excretion. In this study, we examined SNAT3, phosphate-dependent glutaminase (PDG), and phosphoenolpyruvate carboxykinase (PEPCK) regulation during a control (0.36%) or low-K(+) (0.02%) diet for 7 or 14 days or a control (20%) or high-protein (50%) diet for 7 days. MA was induced in control and low-K(+) groups by addition of NH(4)Cl. Urinary ammonium excretion increased during MA, after 14-day K(+) restriction alone, and during high protein intake. SNAT3, PDG, and PEPCK mRNA abundance were elevated during MA and after 14-day K(+) restriction but not during high protein intake. SNAT3 protein abundance was enhanced during MA (both control and low K(+)), after 14-day low-K(+) treatment alone, and during high protein intake. Seven-day dietary K(+) depletion alone had no effect. Immunohistochemistry showed SNAT3 staining in earlier parts of the proximal tubule during 14-day K(+) restriction with and without NH(4)Cl treatment and during high protein intake. In summary, SNAT3, PDG, and PEPCK mRNA expression were congruent with urinary ammonium excretion during MA. Chronic dietary K(+) restriction, high protein intake, and MA enhance ammoniagenesis, an effect that may involve enhanced SNAT3 mRNA and protein expression. Our data suggest that SNAT3 plays an important role as the glutamine uptake mechanism in ammoniagenesis under these conditions.

Index of Suspicion

Index of Suspicion

POTASSIUM depletion and kidney function.

Potassium Depletion and Kidney Function Get access Nutrition Reviews, Volume 14, Issue 11, November 1956, Pages 331–332, https://doi.org/10.1111/j.1753-4887.1956.tb01447.x Published: 01 November 1956

Irbesartan and Hydrochlorothiazide Association in the Treatment of Hypertension

Blood pressure (BP) is one of the most important and common vascular risk factors but it is often poorly controlled. Inhibition of the renin-angiotensin-aldosterone system (RAAS) provides beneficial effects in hypertensives. The association of low-dosed diuretics in combination with RAAS blocking agents allows maximum benefit from potassium depletion and control of compensatory increase in renin secretion, so increasing the efficacy and safety of RAAS blockers. Irbesartan is a potent and selective angiotensin II subtype 1 receptor antagonist indicated for use in patients with hypertension, including those with type 2 diabetes mellitus and nephropathy. Once-daily irbesartan administration provides 24h control of BP. In patients with mild-to-moderate hypertension, irbesartan was as effective as enalapril, atenolol and amlodipine, and more effective than losartan and valsartan in terms of absolute reduction in BP and response rate. Irbesartan also induced regression of left ventricular hypertrophy. Moreover, irbesartan 300 mg/day exerts a significant renoprotective effect in hypertensive type 2 diabetic patients. The relative risk of doubling of serum creatinine was significantly lower with irbesartan than amlodipine or placebo. Irbesartan was also effective in non-diabetic nephropatic patients. Moreover, irbesartan has peroxisome proliferator-activated receptor agonistic effects in in vitro studies, and it also demonstrated beneficial effects on inflammatory markers of atherosclerosis and endothelial function. The overall incidence of adverse events is similar to that of placebo. A fixed dose of hydrochlorothiazide (HCTZ) and irbesartan shows additive antihypertensive effect in a dose dependent manner up to HCTZ 25 mg and irbesartan 300 mg with high tolerability in diverse patient groups. Combination effects on end organ protection must be evaluated by broad spectrum studies. Ongoing trials about irbesartan and its combination with diuretics may provide necessary data to interpret the value of this association among others.

Metabolic Enzymes, Antioxidants, and Cytoskeletal Proteins Are Significantly Altered in Vastus Lateralis Muscle of K-Depleted Cadaveric Subjects

Molecular mechanisms underlying myopathy caused by prolonged potassium (K) depletion remain poorly understood. In the present study, we examined proteome profile of vastus lateralis muscle obtained from cadaveric subjects who had K depletion (KD) (muscle K<80 micromol/g wet weight) compared to those who had no KD (NKD) (muscle K>or=80 micromol/g wet weight) (n=6 per group). Muscle proteins were extracted, resolved by 2-DE, and visualized with CBB-R250 stain. Spot matching and intensity analysis revealed significant changes in levels of 11 (6 increased and 5 decreased) protein spots in the KD group. Q-TOF MS and MS/MS analyses identified these altered proteins as metabolic enzymes (aldehyde dehydrogenase 1A1, uridine diphosphoglucose pyrophosphorylase, enolase 1, cytosolic malate dehydrogenase, and carbonic anhydrase III), antioxidants (peroxiredoxin-3 isoform b), cytoskeletal proteins (slow-twitch skeletal troponin I and myosin light chain 2), and others. These altered proteins are involved in many cellular functions, including bioenergetics, acid-base regulation, oxidative stress response, and muscle contractility. Validation was done by Western blot analysis, which confirmed the increased level of peroxiredoxin-3 and decreased level of troponin-I in the KD muscle. Linear regression analysis also revealed a significant negative correlation between peroxiredoxin-3 level and muscle K content (r=-0.887; p<0.001), as well as a significant positive correlation between troponin-I level and muscle K content (r=0.618; p<0.05). Our results implicate the important roles these altered proteins play in the development of KD-associated myopathy.

Crise cœliaque associée à une tétraplégie par hypokaliémie de déplétion révélatrice d’une maladie cœliaque

Introduction Adult cœliac disease revealed by cœliac crisis and quadriplegia due to potassium depletion is an extremely rare situation. Case report A 26-year-old woman presented with a suddenly developed weakness of all four limbs and a severe diarrhea. Authors emphasize cœliac crisis, which is a presenting feature of cœliac disease, characterized by acute diarrhea with life-threatening acid base and electrolyte abnormalities. The patient improved with correction of hypokalemia and gluten-free diet. Conclusion A severe acute diarrhea with metabolic and systemic complications, the so-called cœliac crisis, is a possible presenting clinical feature of a previously undiagnosed adult celiac disease.

Altered Renal Expression of Na+ Transporters and ROMK in Protein-Deprived Rats

Potassium depletion has been associated with altered sodium reabsorption in tubule segments. We studied if the altered abundance of Na⁺ transporters and ROMK are associated with distal potassium secretion that contributes to the development of hypokalemia in protein-deprived rats. After weaning, Wistar rats were fed with a low-protein diet (8%, LP) for 14 days and then recovered with a normal-protein (NP) diet (24%, RP). An age-matched control group was fed with an NP diet (24%, NP). We showed hypokalemia, lower glomerular filtration rate and higher FEK⁺ in the LP group. Immunoblotting revealed that the type 3 Na⁺/H⁺ exchanger in the cortex was decreased in the LP group. However, the type 2 Na⁺-K⁺-2Cl^– cotransporter was increased in the outer stripe of the outer medulla in the LP group. The abundance of the aldosterone-regulated Na⁺-Cl^– cotransporter (NCC) and epithelial Na⁺ channel (ENaC) was higher in the LP group and was associated with higher plasma aldosterone level. ROMK protein levels were increased. Na⁺/K⁺-ATPase protein levels were the same in both groups. After the recovery period, the expression of Na⁺ transporters and ROMK returned to control values. We conclude that increased expression of NCC, ENaC subunits, and ROMK contributed to distal potassium secretion leading to enhanced potassium excretion, which may explain the hypokalemia resulting from LP feeding. A role of aldosterone may be suggested.

Lithogeochemistry of the Collahuasi porphyry Cu–Mo and epithermal Cu–Ag (–Au) cluster, northern Chile: Pearce element ratio vectors to ore

Abstract Lithogeochemical vectors to ore-bodies are obscured by the variety of lithological units and the alteration events that have affected them. In the magmatic-hydrothermal context, Pearce element ratio (PER) analysis can be a cost-effective lithogeochemical technique that identifies and eliminates non-hydrothermal sources of variation, thus permitting the definition of material transfer related only to hydrothermal alteration. Dedicated PER diagrams for mafic and felsic lithologies in the world-class porphyry Cu–Mo and epithermal Cu–Ag (–Au) cluster of the Collahuasi district, I Region, northern Chile, effectively model background variability and discriminate between fresh or propylitically altered rocks and those with a hydrolytic alteration overprint. Furthermore, PER diagrams allow for the definition of an alteration index (AI) that quantifies the degree of metasomatic exchange during hydrolytic alteration of a particular rock. Plots of different PER values against the AI show that potassium enrichment during hydrolytic alteration was followed by potassium, calcium and sodium depletion as a result of the destruction of feldspars during sericitic and later argillic alteration. Although PER plots record no mass transfer processes involving major elements during propylitic alteration, the integrated AI for both mafic and felsic units spatially defines the major alteration centres within the district.

Effects of vanadate and potassium depletion on renal H, K-ATPase protein expression.

Background: Vanadate (V) inhibits while potassium (K) depletion stimulates collecting tubule H, K-ATPase activity. In the presence of V, K depletion could not restore the decreased H,K-ATPase activity. The effects of V and K depletion on renal H,K-ATPase protein expression might explain such observation. Objective: To examine the effects of V and K depletion on renal H,K-ATPase protein expression. Methods: Rats treated with normal saline solution (NSS) or V (5 mg/kg body weight) received either normal potassium (NK) or low potassium (LK) diet for 10 days. Protein expressions of renal H,K-ATPase α 1 and α 2 isoforms were determined by immunohistochemistry. Results: Both NK and LK animals treated with V had significantly increased vanadium levels in serum, urine, and renal tissues. LK diet caused hypokalemia. Animals treated with LK and V showed progressive hypokalemia. LK stimulated renal H,K-ATPase α 1 protein expression in both cortex and medulla but enhanced H,K-ATPase α 2 protein expression only in the cortex. Vanadate did not affect H,K-ATPase α 1 protein expression in both NK and LK groups. Vanadate unaltered H,K-ATPase α 2 protein expression in NK animals but could attenuate the increased expression in LK group. Conclusion: The magnitude of direct inhibitory effect of V on renal H,K-ATPase activity with small suppressive effect on protein expression is greater than the stimulatory effect of K depletion on H,K-ATPase activity and protein expression.

Endocytic regulation of TGF-β signaling

Transforming growth factor-beta (TGF-beta) signaling is tightly regulated to ensure its proper physiological functions in different cells and tissues. Like other cell surface receptors, TGF-beta receptors are internalized into the cell, and this process plays an important regulatory role in TGF-beta signaling. It is well documented that TGF-beta receptors are endocytosed via clathrin-coated vesicles as TGF-beta endocytosis can be blocked by potassium depletion and the GTPase-deficient dynamin K44A mutant. TGF-beta receptors may also enter cells via cholesterol-rich membrane microdomain lipid rafts/caveolae and are found in caveolin-1-positive vesicles. Although receptor endocytosis is not essential for TGF-beta signaling, clathrin-mediated endocytosis has been shown to promote TGF-beta-induced Smad activation and transcriptional responses. Lipid rafts/caveolae are widely regarded as signaling centers for G protein-coupled receptors and tyrosine kinase receptors, but they are indicated to facilitate the degradation of TGF-beta receptors and therefore turnoff of TGF-beta signaling. This review summarizes current understanding of TGF-beta receptor endocytosis, the possible mechanisms underlying this process, and the role of endocytosis in modulation of TGF-beta signaling.

Endothelial Cell Protein C Receptor Cellular Localization and Trafficking

Endothelial cell protein C receptor (EPCR) is the cellular receptor for protein C (PC) and activated protein C (APC). Recent studies from others and us showed that EPCR also acts as a cellular binding site for factor VII (FVII) and activated factor VII (FVIIa). Although much is know about the biochemistry and pathophysiological importance of EPCR, little is know how EPCR interaction with its ligands on cell surfaces affects its expression and facilitate internalization of the ligands. The present study was undertaken to characterize cellular localization and trafficking of EPCR and investigate how FVIIa or APC binding to EPCR influences these processes. The studies employed two cell model systems - primary cultured human umbilical endothelial cells (HUVEC) and CHO cells stably transfected with EPCR. Cellular localization of EPCR and its trafficking was analyzed by immunofluorescence confocal microscopy or monitoring the expression of EPCR tagged with green fluorescence protein (GFP). EPCR endocytosis was evaluated by biotinylation of cell surface proteins with NHS-SS- biotin, followed by monitoring the protection of biotinylated EPCR from a membrane-impermeable reducing agent. FVIIa and APC internalization and recycling was evaluated by monitoring the uptake/release of 125I-labeled ligands or following the intracellular routing of fluorescent dye (AF488)-conjugated ligands added to EPCR expressing cells. Data from these studies showed that a majority of EPCR is localized on the cell surface and distributed in a patchy and punctuate manner. Immunostaining of HUVEC and CHO-EPCR cells with EPCR mAb and caveolin-1 antibodies showed a high degree of co-localization of EPCR and caveolin-1. Depletion of cholesterol from the plasma membrane, which disrupts caveolae, by ß methyl cyclodextrin reduced the extent EPCR and caveloin-1 colocalization. These data indicate EPCR on the cell surface predominantly localizes in caveolae. Inside the cell, EPCR is mainly localized in a small perinuclear structure, which is the site of centrosome. Colocalization of EPCR with tubulin (a marker for centrosome) and rab 11 (a marker of recycling compartment, REC) revealed that EPCR is localized actually in the REC and not in the centrosome. A small fraction of EPCR is also localized in endosomes as evident from colocalization of EPCR with EEA1 and Rab5, early endosome markers. Chasing the cell surface biotinylated proteins showed no significant increase in the biotinylated EPCR in the intracellular pool of proteins, which indicate that EPCR is not actively endocytosed constitutively or that the internalized EPCR is immediately recycled back to the cell surface. FVIIa or APC binding to EPCR promoted the EPCR endocytosis. The endocytosed receptors were first observed in proximity of the plasma membrane after 10 min and by 30 to 60 min most of the endocytosed EPCR was accumulated in the REC. The internalized FVIIa or APC appeared to follow the same route of the endocytosed EPCR. Proteolytically inactive FVIIa or APC behaved same as FVIIa or APC in promoting EPCR endocytosis and its trafficking. EPCR-dependent FVIIa or APC internalization is a dynamin-dependent process as the inhibition of the GTPase activity of dynamin by a specific inhibitor (Dynasore) completely abrogated their internalization and accumulation in the REC. Additional studies revealed that disruption of coated-pit pathway by potassium depletion blocked the endocytosis of transferrin, a classic marker for endocytosis via clathrin-dependent coated-pit pathway, but had no effect on EPCR-dependent FVIIa or APC internalization. In contrast, disruption of caveolae by cholesterol depletion blocked the internalization of FVIIa but not transferrin. Rab11 dominant negative mutant form (S25N) prevented the passage of the endocytosed EPCR or the internalized FVIIa or APC into the REC. After peaking at 30 min, the amount of both the ligands and the receptor in the REC gradually decreased, and some of the internalized ligand re-appeared at the cell surface. Overall the data provided herein suggest that FVIIa or APC binding to EPCR, independent of their protease activity, promotes EPCR endocytosis via the dynamin-dependent caveolar pathway and the activation of rab11 by GTP is required for exit of the endocytosed receptor or the ligands from sorting endosomes to the recycling compartment.

Effects of saline root environment (NaCl) on nitrate and potassium uptake kinetics for rose plants: a Michaelis–Menten modelling approach

Greenhouse-grown cut flower roses are often irrigated with moderately saline irrigation water. The salt/ballast ions are either present initially in poor quality raw water or reclaimed municipal water, or accumulated in greenhouse irrigation water that is captured and reused. Such ions can inhibit root absorption of essential nutrients. The objective of this work was to quantify the influence of NaCl concentration on the uptake of nitrate and potassium by roses and develop a predictive model of uptake inhibition based on NaCl, NO3 −, and K+ concentration. One year-old rose plants (Rosa spp. ‘Kardinal’ on ‘Natal Briar’ rootstock) were moved into growth chambers where nitrogen and potassium depletion were monitored during 6 days. Eight different initial NaCl treatments varying from zero to 65 mol m−3 were used and within these there were two initial NO3 − and K+ concentrations: high concentration (HC, 7.0 mol m−3 and 2.6 mol m−3 NO3 − and K+ respectively) or low concentration (LC, 3.5 mol m−3 and 1.3 mol m−3 NO3 − and K+ respectively). Plant NO3 − uptake was negatively affected by NaCl concentration. NO3 − maximum influx (Imax) declined from 5.1 µmol to 2.5 µmol per gram of plant dry weight per hour as NaCl concentration increased from zero to 65 mol m−3. A modified Michaelis–Menten (M–M) equation taking into account inhibition by NaCl provided the best fit for NO3 − uptake in response to varying NaCl concentration. K+ uptake was unaffected by NaCl concentration. A M–M equation that did not include inhibition was suitable for describing K+ uptake at varying NaCl concentration. The resulting empirical models could assist with decision making, such as: adjustment of NO3 − fertilization based on NaCl concentration, necessity of water desalinization, or determination of the desired leaching fraction.

The Value Of High Dose Frusemide In The Management Of 350 Open Prostatectomies

Background: The use of frusemide in open and closed prostatectomy has provided a distinct advance over osmotic diuretics. Objective: To report our experience in the use of high dose infusion of frusemide in the postoperative management of 350 open prostatectomy and discuss its benefits. Patient and Methods: The study included 350 consecutive patients with benign prostatic enlargement who were managed with open prostatectomy and high dose frusemide infusion for bladder irrigation. The age ranged between 49 and 90; the mean age was 61 years. 330 (94.0%) patients presented with urine retention. Other associated medical and surgical conditions were adequately treated before, during and after prostatectomy. Suprapubic prostatectomy was performed on 319 (91.1%) patients while retropubic prostatectomy was on 31 (8.9%) patients. General anaesthesia was administered on 196 (54.6%), spinal analgesia on 139 (39.7%) and epidural analgesia on 15 (4.3%) patients. Blood transfusion, intravenous fluid and frusemide were given during and after operation to replace losses and maintain urine flow. A group of 100 consecutive prostatectomy were given Darrows solution, 1 litre in the first day and 1 litre in the second day following operation. Patients were carefully monitored during the 48 hours of intravenous fluid and frusemide infusion regime. Fluid intake, urine output, sodium and potassium losses in urine were studied in both group of patients. Frusemide infusion regime was carefully followed. Fluid intake regulated to be at least 500mls ahead of urine output during the infusion regime. Frusemide administration was discontinued at the end of the first 24 hours following operation and oral fluids commenced. Results: Intraoperatively, 268 (76.6%) patients were transfused with one unit of blood each; 40 (11.4%) patients received 2 units of blood each while 42 (12.0%) patients did not require blood transfusion. The average daily urinary electrolyte losses were 450 mmol of sodium and 32 mmol of potassium. The levels of serum sodium and potassium remained within the normal range in all patients. In the first 24 hours fluid intake ranged between 5.5 and 8.5 litres while urine output ranged from 3.8 to 6.4 litres. 28 (8.0%) patients complained of nausea and 10 (2.9%) vomited each once following the bolus intravenous injection of 40mg of frusemide. Two patients died on the 6th and 8th postoperative days respectively. Mortality was 0.6 percent. Conclusion: The use of high dose frusemide infusion in open prostatectomy is simple to administer, safe, cost effective and not associated with significant potassium depletion. Keywords: Open prostatectomy, Fursemide infusion, Postoperative managementSahel Medical Journal Vol. 11 (1) 2008: pp. 28-33

Thiazide Diuretics: 50 Years and Beyond

Since the introduction of chlorothiazide into clinical practice in 1958, thiazide-type diuretics have weathered decades of criticism and controversy. Fifty years later, they remain the single most important class of antihypertensives available. Numerous clinical trials across broad populations consistently demonstrate superior reductions in cardiovascular outcomes with thiazide-based regimens and most notably using the thiazide-like diuretic, chlorthalidone. Recent evidence suggests there may be important differences among thiazides that favor chlorthalidone due to its longer half-life and duration of action. Despite their proven record, thiazide diuretics continue to be scrutinized for their well-known adverse metabolic profile, especially hypokalemia. Glucose intolerance and incident diabetes with diuretic therapy has received significant attention; however, evidence from the ALLHAT study and others indicate the reductions in cardiovascular outcomes with thiazides are also observed in diabetics. Potassium depletion may be associated with diuretic dysglycemia. To minimize the adverse metabolic profile of thiazides, clinicians should preferentially use low doses. Combinations with potassium- sparing agents, or with renin-angiotensin system drugs such as angiotensin-converting enzyme inhibitors or angiotensin receptor blockers should also be considered. The last fifty years has seen remarkable advances in our understanding and treatment of hypertension and thiazides remain the most important pharmacologic advancement in our therapy of hypertension. Keywords: Diuretics, hypertension, antihypertensive therapy, hydrochlorothiazide, chlorthalidone

Altered neuronal expression of TASK1 and TASK3 potassium channels in rodent and human autoimmune CNS inflammation

Multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are characterized by T cell-mediated autoimmune inflammation of the central nervous system (CNS) leading to oligodendrocyte loss and demyelination accompanied by neuronal cell death. Neuronal TWIK-related acid-sensitive potassium (TASK) channels allow the regulated efflux of potassium ions. These channels might either protect neurons in the inflamed CNS by modulating electrical excitability or even contribute to inflammatory neurodegeneration mediating intracellular potassium depletion. Using a combination of in-situ-hybridisation and immunofluorescence staining, we found increased neuronal expression of TASK1 and TASK3 channels in the optic nerve and decreased expression in the spinal cord and thalamus of rats undergoing MOG-induced EAE. Inflammatory plaques of human MS patients displayed profoundly lowered expression of both TASK isoforms. Thus, regulated expression of TASK channels might contribute to a molecular switch between death and survival of neurons in autoimmune CNS inflammation.

Abdominal Obesity Is Associated With Potassium Depletion and Changes in Glucose Homeostasis During Diuretic Therapy

The activation of the renin-angiotensin system (RAS) is an important mechanism that contributes to hypertension in obese individuals. Thiazide diuretics also activate the RAS in response to volume contraction and can lead to a decrease in serum potassium values and glucose metabolism abnormalities. To evaluate the impact of abdominal obesity on potassium depletion and glucose homeostasis in hypertensive patients receiving thiazide therapy, the authors studied 329 hypertensive patients without known diabetes or impaired renal function. Patients were stratified into 2 major groups according to whether they used thiazide diuretic therapy, and each group was further divided in 2 subgroups according to the presence of abdominal obesity. The authors demonstrated that obese patients receiving diuretic therapy had lower plasma potassium levels and higher glucose values compared with nonobese patients receiving diuretic therapy. In conclusion, abdominal obesity predisposes to potassium depletion during diuretic therapy in association with effects on glucose homeostasis.

Hypokalemic paralysis is not just a hypokalemic paralysis

Although the commonest form of hypokalemic paralysis is the hereditary variety, some patients during course of thyrotoxicosis or with chronic potassium depletion, may exhibit episodic weakness. Approach to the patient with hypokalemic paralysis should be a careful search for the etiology and potassium replacement therapy. In this report, two hypokalemic paralysis cases are described. Case 1 is a 29-year-old Caucasian male who developed thyrotoxic periodic paralysis. Case 2 is a 50-year-old female who experienced hypokalemic paralysis due to primary aldosteronism. Hypokalemic paralysis usually carries an underlying secret problem. Emergency department workers should give importance to etiological differentiation.

Thiazide-type diuretics and beta-adrenergic blockers as first-line drug treatments for hypertension.

Systemic arterial hypertension affects 72 million US adults and an additional hundreds of millions of persons worldwide.1,2 Most of these are candidates for pharmacological treatment to reduce risk of cardiovascular disease (CVD) events, based primarily on a very large body of epidemiological and intervention research in humans. Because of this high prevalence and the cardiovascular consequences of untreated or inadequately treated hypertension, the selection of drugs for initial and continuing, long-term treatment has large public health and economic implications. Fortunately, such decisions and the expert recommendations that seek to guide them can call on evidence from 4 decades of randomized multicenter clinical trials evaluating effects of treatment on clinical CVD. We summarize that evidence in this article, in approximate chronological order, and we comment on the related treatment guidelines. We close with some of the major clinical questions yet to be resolved. Response by Messerli et al p 2705 Before the current era beginning in the early 1990s of emphasis on positive-control trials, which directly compare different drug regimens, there were 3 decades of trials that compared an active regimen with placebo or, in a few cases, “usual care.” For most of this period, the mainstay of treatment was generally a thiazide-type diuretic (hereinafter called thiazides) or, to a lesser extent, a β-adrenergic blocker (termed β-blockers). With few exceptions, these trials, especially those with high statistical power and thiazide-based regimens, showed benefit for CVD outcomes.3–8 This evidence, which provided a basis for recommending thiazides or β-blockers as first-step drugs in most editions of US guidelines through 1997,9 needs to continue to be given due weight in practice and practice guidelines. The largest and most consistent benefits from the earlier trials were for stroke and (where reported) heart failure. Benefits for coronary heart disease (CHD) were less clear, …

Cesium adsorption and distribution onto crushed granite under different physicochemical conditions

The adsorption of cesium onto crushed granite was investigated under different physicochemical conditions including contact time, Cs loading, ionic strength and temperature. In addition, the distribution of adsorbed Cs was examined by X-ray diffraction (XRD) and EDS mapping techniques. The results showed that Cs adsorption to crushed granite behaved as a first-order reaction with nice regression coefficients ( R 2 ≧ 0.971). Both Freundlich and Langmuir models were applicable to describe the adsorption. The maximum sorption capacity determined by Langmuir model was 80 μmol g −1 at 25 °C and 10 μmol g −1 at 55 °C. The reduced sorption capacity at high temperature was related to the partial enhancement of desorption from granite surface. In general, Cs adsorption was exothermic (Δ H < 0, with median of −12 kJ mol −1) and spontaneous (Δ G < 0, with median of −6.1 at 25 °C and −5.0 kJ mol −1 at 55 °C). The presence of competing cations such as sodium and potassium ions in synthetic groundwater significantly reduces the Cs adsorption onto granite. The scanning electron microscopy–energy dispersive X-ray spectroscopy (SEM/EDS) mapping method provided substantial evidences that micaceous minerals (biotite in this case) dominate Cs adsorption. These adsorbed Cs ions were notably distributed onto the frayed edges of biotite minerals. More importantly, the locations of these adsorbed Cs were coincided with the potassium depletion area, implying the displacement of K by Cs adsorption. Further XRD patterns displayed a decreased intensity of signal of biotite as the Cs loading increased, revealing that the interlayer space of biotite was affected by Cs adsorption.