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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper is intended to give a review of the etiology and symptoms of potassium deficiency in man, as an introduction to the section on potassium and cardiac arrhythmias of this symposium. A review is given of different conditions where hypokalemia and/or total potassium deficiency is or might be part of the clinical picture, such as conditions with insufficient dietary intake, gastrointestinal potassium losses (e.g. vomiting, fistulas, malabsorption, abuse of laxatives and diarrhea), and renal potassium losses (e.g. primary and secondary hyperaldosteronism, Cushing's syndrome, intake of licorice, diabetic coma, renal disease, diuretic treatment and l-dopa treatment). Common symptoms of hypokalemia and/or potassium deficiency are reviewed as well, such as general and unspecific symptoms (e.g. tiredness, lack of concentration, lack of appetite and vomiting), and symptoms from the heart, kidneys and skeletal muscle.
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PMID:Hypokalemia--clinical spectrum and etiology. 702 Mar 49

This study compares the frequency of dialysis disequilibrium symptoms (DDS), in 17 stable non-diabetic chronic hemodialysis patients, during a period using low glucose (200 mg/100 ml) dialyzate to a similar period using a glucose free dialyzate. There was a significant decrease in the total number of symptoms as well as the frequency of headache and post-dialysis fatigue during the low glucose period as compared to the glucose free period. The decrease in nausea or vomiting, and cramps was not significant while frequency of hypotension was unchanged. Evaluation of serum sodium, potassium, BUN, glucose and osmolarity did not reveal significant differences during the two periods. Dialysis with a low glucose bath produces less DDS than glucose free dialyzate.
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PMID:Improvement in disequilibrium symptoms during dialysis with low glucose dialyzate. 714 23

It is generally assumed that noises have a detrimental effect when the cochlear receptor is overloaded and, more specifically, when the cochlear microphonic (CM) fails to increase linearly with intensity. In order to investigate further the relations between the nonlinearity of CM and damage to the cochlea, a series of experiments was carried out on guinea pigs to relate the short-term CM depression following the presentation of noises or tones with the nonlinearity and the assymmetry. The asymmetrical non-linearity of CM was measured in tracing the input-out functions and also the wave-forms. Two other important tests of the asymmetrical nonlinearity were used: the measure of interference and of summating potential (SP DIF). The results show that the fatigability is greater when there is a large negative asymmetry or a large negative SP. Variations in asymmetry and in SP were observed among individuals. Other changes of symmetry were provoked by asphyxia or by introducing solutions of KCl in the perilymph. These changes were well correlated with the fatigability. These results are interpreted in a model of the cochlear transducer derived from the model of Davis. The assymetry of a flux of potassium ions between endolymph and the hair cells is assumed to be responsible for the alterations associated with cochlear fatigue and trauma.
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PMID:Relations between cochlear fatigue and the asymmetrical nonlinearity of the cochlear microphonics. 736 35

Although essential hypertension is usually defined as a hemodynamic disorder, it is expressed differently among individuals and varies during progression of the disease state. Therefore, various types of treatment can be envisioned. The use of selective I1-imidazoline-receptor agonists to modulate I1-imidazoline receptors involved in the central regulation of blood pressure has led to the introduction of a novel class of centrally acting antihypertensive drugs. Moxonidine, a representative molecule of this class, dissociates between a 10% alpha 2-adrenoceptor-agonist action linked with side effects such as fatigue or dry mouth, and a 90% specific antihypertensive action resulting from its selective agonistic action at I1-imidazoline receptors. Clinical experience is based on more than 2,000 patients and volunteers, and long-term efficacy has been demonstrated in about 500 patients who received a daily dose of moxonidine 0.2-0.4 mg. Moxonidine produces a pronounced reduction in peripheral vascular resistance without reflex tachycardia, accompanied by reduced plasma norepinephrine concentration and plasma-renin activity. Cardiovascular responses to exercise and standing remain nearly normal, and serious or life-threatening side effects, particularly the sympathetic overactivity that can occur on sudden withdrawal of other centrally acting agents, are never observed. In addition, moxonidine behaves neutrally with respect to plasma levels of cholesterol, potassium and glucose, glucose and lipid metabolism, and renal function, and can be administered without complication to patients with asthma or certain other diseases. Studies with magnetic resonance imaging have shown that moxonidine significantly reduces left ventricular mass, an indicator of left ventricular hypertrophy (LVH), within a 6-month treatment period, an effect that coincided with decreased plasma concentrations of catecholamines and renin. Comparisons between moxonidine and other well-established antihypertensive drugs such as nifedipine, atenolol, or angiotensin-converting enzyme inhibitors showed equal effectiveness in lowering blood pressure, whereas the adverse events profile always favored moxonidine. Considering its efficacy, safety, and specific effects (e.g., its ability to reduce LVH), moxonidine meets the criteria satisfied by other currently prescribed antihypertensive drugs. Because of its especially favorable benefit-to-risk ratio, moxonidine should be recommended as first-line treatment of hypertension and may also be useful in treating related problems such as LVH, coronary artery disease, and ventricular premature beats.
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PMID:I1-imidazoline-receptor agonists in the treatment of hypertension: an appraisal of clinical experience. 753 26

Prazosin (an alpha-1-adrenergic blocker) and cromakalim (potassium channel opener), given alone, induced significant fatigue of the urethral sphincter at a concentration of 10(-4) M; both drugs combined achieved a significant sphincteric fatigue at a concentration of 10(-5) M each. To 10(-4) M hexamethonium (ganglionic smooth muscle blocker) and 10(-4) M decamethonium (nicotinic blocker of striated muscle) the striated urethral sphincter responded like striated muscle with no detectable function of its smooth muscle component. Therefore, the striated component seems to play a dominant role in sphincteric function. With calcium depletion or in the presence of a calcium channel blocker (10(-4) M nifedipine) the urethral sphincter showed a relative enhancement of response to electrical field stimulation when compared with smooth and skeletal muscle, whose responses were both significantly reduced. This phenomenon could not be explained with calcium-dependent, inhibitory, nitric oxide-releasing nerves, as the NO-synthase blocker N-nitro-L-arginine (10(-5) M to 5 x 10(-5) M) failed to induce the enhancement of sphincter contraction during electrostimulation found with calcium depletion. Still, NO-releasing nerves might play a role in sphincteric relaxation because sodium nitroprusside (10(-5) M) induced a significant relaxation of the urethral sphincter precontracted with 80 mM potassium. The potential to weaken sphincteric closure with drugs, exemplified by the results obtained in response to prazosin and cromakalim, would represent a therapeutic advance in the patient with neurogenic bladder dysfunction.
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PMID:Response of guinea pig smooth and striated urethral sphincter to cromakalim, prazosin, nifedipine, nitroprusside, and electrical stimulation. 754 86

This review summarizes the main cellular mechanisms involved in potassium regulation in plasma and skeletal muscle during exercise. The effects of exercise-induced hyperkalemia and post-exercise hypokalemia on the cardiac action potential are reviewed in light of recent research on Na+ and K+ channel activity. Specific consideration is given to K+ release from contracting skeletal muscle, K+ uptake by contracting skeletal muscle, K+ uptake by non-contracting tissues during the period of exercise, and K+ uptake by skeletal muscle recovering from contractile activity. The onset of exercise is associated with a net release of K+ from contracting skeletal muscle that results in an increase in plasma [K+]. Resultant decreases in intracellular [K+] and increases in interstitial [K+] in contracting skeletal muscle have been implicated in the fatigue process. The rate and magnitude of increase in plasma [K+] is dependent on exercise intensity, trained state of the individual, and on drugs such as beta-adrenoceptor blockers and caffeine. During exercise, the uptake of K+ from the blood by non-contracting tissues may be important in preventing plasma [K+] from rising to excessive levels that will impair skeletal muscle and myocardial excitability and contractility. Cessation of exercise results in a rapid decrease in plasma [K+], often to 3 mEq/l or less with intense exercise, that may be maintained for prolonged periods. The rapid increases and decreases in plasma [K+] with onset and cessation of exercise, respectively, has been implicated in altered myocardial function and sudden cardiac death. Recent studies suggest that increases in catecholamines during exercise are cardioprotective to the arrhythmogenic effects of hyperkalemia.
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PMID:Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle. 756 98

Potassium release from contracting skeletal muscle cells facilitates ongoing muscle contraction but may also lead to muscular fatigue. This review focuses on the effects of altered physical activity on K+ regulation during exercise, with special emphasis on K+ regulation in humans. Endurance and sprint training specifically enhance prolonged and high intensity exercise performance, respectively. Both forms of training reduce the exercise-induced rise in plasma [K+] at the same absolute exercise work rate and duration and increase the total concentration of Na+,K+ pumps in trained human muscle by approximately 15%. However, the increased pump density has not been proven to account directly for either the reduced hyperkalaemia or the improved exercise performance after training. The most likely factor accounting for the improved K+ regulation after training is an increased activation of Na+,K+ pumps during exercise, but this is not due to increased circulating catecholamine concentrations after training. A chronic reduction in physical activity reduces the muscle Na+K+ pump concentration in animal models, with an augmented exercise-induced rise in plasma [K+]. Thus, physical training enhances, whilst inactivity impairs K+ regulation during exercise, consistent with the improved exercise performance after physical training and the impaired performance with inactivity.
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PMID:Effects of training on potassium homeostasis during exercise. 756 6

Seven Arabian horses performed a standard incremental exercise test on a high-speed treadmill at 6% slope then were randomly assigned to two diets, a control diet of ground hay and concentrates and a similar diet with 10% added fat (by weight). Horses were sprint-trained 4 d/wk, and two additional exercise tests were performed at 5-wk intervals. Heart rates and rectal temperatures were monitored and venous blood samples were collected at rest and at each speed increment. Whole blood was analyzed for glucose, lactate, and hemoglobin concentrations, and plasma was analyzed for pH, pCO2, albumin, total protein, and sodium, potassium, and chloride concentrations. Bicarbonate concentration ([HCO3-]) and strong ion difference ([SID]) were calculated, and total weak acid ([Atot]) was estimated from total protein. During exercise, there were increases in plasma sodium and potassium concentrations (P < .001), whole blood lactate and glucose (P < .001), and hemoglobin concentrations (P < .01). There were decreases in plasma pH, [HCO3-], and chloride concentrations (P < .001). The decrease in plasma pH was associated with changes in [SID] and [Atot] that combined to offset a decrease in pCO2. After sprint training, heart rates at rest and during submaximal exercise were decreased (P < .01), whereas heart rates at the end of exercise were increased (P < .05). Sprint training also increased workrate and estimated oxygen consumption at a heart rate of 200 beats/min (P < .001). Training increased the duration of exercise and the speed attained at the end of exercise (P < .05). Training increased the blood hemoglobin response to exercise and decreased the pCO2 response (P < .01). There were diet x training interactions for pH, pCO2, and [SID] (P < .05). Horses consuming the high-fat diet had higher blood glucose during both standard exercise tests and higher lactate concentrations at fatigue (P < .05) during the last test. Fat adaptation involving sprint training of horses may influence glucolysis at the level of pyruvate during an incremental exercise test.
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PMID:Acid-base variables during incremental exercise in sprint-trained horses fed a high-fat diet. 759 85

High-frequency fatigue (HFF), the decline of force during continuous tetanic stimulation (lasting 4-40 s), was studied in isolated bundles of rat skeletal muscle fibers. HFF was slower in slow-twitch soleus fibers than in fast-twitch red or white sternomastoid fibers; denervation accelerated fatigue in soleus. Maximal 200-mmol/L potassium contractures of normal amplitude were induced in fatigued fibers, suggesting that crossbridge cycling and the voltage activation of excitation-contraction coupling could still occur maximally, but that activation by action potentials was impaired. An increase in [Na+]o slowed HFF, while a small increase in [K+]o or reduction in [Cl(-)]o accelerated HFF. Increasing the tetanic stimulation frequency exacerbated fatigue. Recovery from HFF proceeded rapidly since force increased markedly within a few seconds when stimulation ceased. These results support the hypothesis that a redistribution of Na+, K+, and Cl- across the transverse tubular membranes during repeated action potential activity induces fatigue by reducing the amplitude and conduction of action potentials.
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PMID:High-frequency fatigue in rat skeletal muscle: role of extracellular ion concentrations. 763 Mar 51

This report presents data on the safety and tolerability of losartan potassium (losartan), a selective antagonist of the angiotensin II AT-1 receptor, in approximately 2,900 hypertensive patients treated in double-blind clinical trials. In these studies, headache (14.1%), upper respiratory infection (6.5%), dizziness (14.1%), asthenia/fatigue (3.8%), and cough (3.1%) were the clinical adverse experiences most often reported in patients treated with losartan. These adverse experiences were also frequently reported in patients receiving placebo: 17.2%, 5.6%, 2.4%, 3.9%, and 2.6%, respectively. Dry cough as an adverse event was reported in 8.8% of patients treated with angiotensin-converting enzyme inhibitors, and in 3.1% and 2.6% of patients treated with losartan or placebo, respectively. Only dizziness was considered "drug-related" more often in losartan-treated (2.4%) than placebo-treated (1.3%) patients. In controlled clinical trials, losartan was better tolerated than other antihypertensive agents as determined by the incidence of patients reporting any drug-related adverse experiences. Rates of discontinuation due to clinical adverse experiences in patients who received losartan monotherapy or losartan+hydrochlorothiazide were 2.3% and 2.8%, respectively, compared with placebo (3.7%). No laboratory adverse experiences were unexpected or of clinical importance. First-dose hypotension rarely occurred with losartan or with losartan plus hydrochlorothiazide, and withdrawal effects such as rebound hypertension were not observed in clinical trials. There were no clinically important differences in the clinical or laboratory safety profiles in the demographic subgroups for age, gender, or race. In controlled clinical trials, losartan demonstrated an excellent tolerability profile.
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PMID:Safety and tolerability of losartan potassium, an angiotensin II receptor antagonist, compared with hydrochlorothiazide, atenolol, felodipine ER, and angiotensin-converting enzyme inhibitors for the treatment of systemic hypertension. 771 81


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