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PubMed1993

Effect of chronic potassium depletion on muscle bioenergetics in rats.

To test the hypothesis of muscle bioenergetic impairment in potassium depletion, chronic potassium-depleted rats and pair-fed control rats were studied with phosphorus 31 nuclear magnetic resonance measurements of leg muscle intracellular pH, phosphocreatine, inorganic phosphate, and adenosine triphosphate at rest and during maximal nontetanic stimulation, 48 hours after a swimming test. The potassium-depleted rats exhibited a significant hypokalemia, a metabolic extracellular alkalosis, and an intracellular acidosis. Their physical endurance was markedly reduced, and they displayed higher plasma creatine kinase levels than the control group. However, the phosphocreatine/inorganic phosphate ratio, which is a measure of the energy reserve of the cell, was similar in both groups at rest and during electrical stimulation and subsequent recovery. Resting muscle glycogen and relative intracellular acidification during stimulation did not differ in the two groups, arguing against an impairment of anaerobic metabolism in potassium depletion. These results indicate that the energy availability of muscle cell is unchanged during potassium deficiency.

Animals↗
PubMedDate not supplied

Age-related changes in renal function, membrane protein metabolism, and Na,K-ATPase activity and abundance in hypokalemic F344 x BNF(1) rats.

BACKGROUND: Potassium depletion is a common electrolyte abnormality in elderly humans, usually as a consequence of diuretic use or poor oral intake. Hypokalemia is associated with a number of changes in renal function and an increase in some renal membrane transporters; its growth-promoting effect in young animals is well known. With aging, the renal adaptation to a number of challenges is often diminished. We hypothesized that aging is related to decreases in renal function, renal membrane protein metabolism, as well as Na, K-ATPase protein abundance and activity in both control animals as well as in those with potassium depletion. OBJECTIVE: We examined the effects of dietary-induced hypokalemia in true-aged nonobese rats (30 months old) on renal function, cortical brush border membrane (BBM) and basolateral membrane (BLM) protein metabolism, and Na,K-ATPase protein abundance and activity. We compared the results obtained to those seen in their 4-month-old counterparts similarly treated. METHODS: Young (4-month-old) and senescent (30-month-old) male Fisher 344 x Brown-Norway F(1) rats (F344 x BNF(1)) were fed either a normal or potassium-deficient diet for 7 days. At 24 h, the U-(14)C-leucine incorporation was measured for determination of protein metabolism in renal BBM and BLM. Cortical BLM vesicle and microdissected proximal convoluted tubule (PCT) Na, K-ATPase activities were determined along with Western blot analysis of the cortical BLM alpha(1) subunit of Na,K-ATPase. Metabolic and renal function parameters were also examined. RESULTS: Hypokalemia caused hyperbicarbonatemia, hyperglycemia, and azotemia, but only in the senescent animals. The aged control rats had a higher basal level of urine volume, ammonium excretion, and fractional excretion of chloride. By contrast, aging in the F344 x BNF(1) rats was associated with a decrease in plasma aldosterone (by 35%) and phosphate (by 40%) levels as compared with their young controls. Hypokalemia resulted in a significant reduction of plasma aldosterone and a rise in muscle sodium concentration in both age groups; it significantly increased renal BBM and BLM protein concentrations in the young group, while these parameters remained unchanged in the senescent rats. The aged potassium-depleted animals showed a 14% decrease in BBM protein biosynthesis, but there were no changes in the young hypokalemic rats. Both potassium-depleted elderly and young rats had a significant reduction (by 33%) in BLM protein biosynthesis. Hypokalemia significantly increased the Na, K-ATPase activity in both cortical BLM vesicles and in microdissected PCT. The percentage increase in microdissected PCT segments (Na,K-ATPase activity) in elderly potassium-depleted animals was significantly less than that seen in hypokalemic young ones. Aging, per se, was associated with decreased basal microdissected PCT Na,K-ATPase activity in control animals. Hypokalemia had no effect on cortical BLM alpha(1) subunit Na, K-ATPase protein abundance in either age group. CONCLUSIONS: The present study provides the first evidence in nonobese aged rats as to the metabolic parameters, renal function, renal cortical membrane protein metabolism, and transporter Na,K-ATPase activity and abundance during potassium depletion. The aged nonobese F344 x BNF(1) rats responded differently from their young nonobese counterparts following potassium depletion. These differences may contribute substantially to the effects often encountered in elderly humans receiving diuretics or having a poor dietary potassium intake.

Age Factors↗
PubMed2000

Gamble and Darrow: pathfinders in body fluid physiology and fluid therapy for children, 1914-1964.

The development of body fluid physiology and fluid therapy in pediatrics has special importance in the history of medicine because this development introduced physiology into clinical practice. James Gamble and Dan Darrow were leaders in this enterprise. Gamble was part of the group John Howland attracted to Johns Hopkins to establish the first organized program for clinical investigators in pediatrics. This group initiated fluid therapy as effective treatment for diarrheal dehydration and, led by Gamble, developed the discipline of body fluid physiology. Gamble was the first to describe the nature of extracellular fluid (ECF) to clinicians, using the new terminology for characterizing electrolytes in solution. In doing so, he became the teacher of body fluid physiology to a generation of medical students. Inexplicably, in his later years he failed to adopt yet newer terminology defining cations, anions, and acid-base status. This failure compromised his legacy. Dan Darrow extended our understanding of how body fluids react to hyper- and hyponatremia and to potassium deficiency. He was the first to add potassium to parenteral fluid therapy. In doing so, he broadened clinicians' understanding of body fluids but changed the emphasis of fluid therapy from rapid ECF restoration to replacement of estimated deficits. Unfortunately, this change in concept, taught by his successors as deficit therapy, slowed the adoption of oral rehydration therapy for treating diarrheal dehydration. The lapses noted for each of these men, now seen in hindsight, pale in comparison to their contributions. Pediatrics, medicine, and surgery are all indebted to the research of each, which emphasized the value of basic physiology in clinical practice.

Body Fluids↗
PubMed1975

[Diagnosis and treatment of disorders of the potassium balance with special reference to infusion therapy].

Following a short review of the physiological regulation of body potassium diagnostic procedures to detect disturbances in potassium balance are cited. The limited value of serum potassium concentration is emphasized. Possible caused of potassium deficiency and prophylactic measures to prevent negative potassium balance are summarized including oral and parenteral potassium administration. A synopsis of the causes of hyperkalemia is followed by a description of therapeutical measures. Chronic hyperkalemia may be treated by oral or rectal administration of ion-exchange resins, while acute lifethreatening hyperkalemia is corrected by infusion of isotonic saline, glucose and insulin, and calcium gluconate as well as by correction of metabolic acidosis with sodium bicarbonate. In patients with intact renal function these measures will generally result in rapid correction of increased serum potassium levels.

Acid-Base Equilibrium↗
PubMed1977

Symptoms and course of chronic hypokalemic nephropathy in man.

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.

Adult↗
PubMed1980

The role of urinary prostaglandin E and cyclic AMP in the polyuria of hypokalemia in rats.

The effect of potassium depletion on urinary prostaglandin E and cyclic AMP excretion was studied in female Sprague-Dawley and in Brattleboro rats. The animals were fed a potassium-free diet for 20 days which resulted in an average decrease in serum potassium of 25% in both strains. In the Sprague-Dawley rats, potassium depletion increased urine volume from 5.5 +/- 0.9 ml/day to 25.9 +/- 3.5 ml/day (p less than 0.001), decreased urinary osmolality from 1483 +/- 87 mosmol/kg H2O to 372 +/- 12 mosmol/kg H2O (p less than 0.001) and suppressed urinary cyclic AMP excretion from 56.95 +/- 3.81 nmoles/day to 0.83 +/- 0.40 nmoles/day (p less than 0.001). Potassium depletion in the Brattleboro rats did not affect these parameters. Excretion of prostaglandin E-like immunoreactivity in urine did not change in either strain with potassium depletion. The findings support the hypothesis that prostaglandins do not play a significant role in the polyuria caused by potassium deficiency in rats. Hypokalemia may cause polyuria by suppression of vasopressin-sensitive cyclic AMP generation, leading to a decrease in water permeability.

Animals↗
PubMed1978

The effect of acid--base changes on skeletal muscle twitch tension.

The effects of acid--base alterations produced by changing bicarbonate (metabolic type), carbon dioxide tension (respiratory type), or both bicarbonate and carbon dioxide tension (compensated type) on skeletal muscle twitch tension, intracellular pH, and intracellular potassium were studied in vitro. Hemidiaphragm muscles from normal rats and rats fed a potassium-deficient diet were used. Decreasing the extracellular pH by decreasing bicarbonate or increasing CO2 in the bathing fluid produced a decrease in intracellular pH, intracellular K+, and muscle twitch tension. However, at a constant extracellular pH, an increase in CO2 (compensated by an increase in bicarbonate) produced an increase in intracellular K+ and twitch tension in spite of a decrease in intracellular pH. The effect on twitch tension of the hemidiaphragms showed a rapid onset, was reversible, persisted until the buffer composition was changed, and was independent of synaptic transmission. It is concluded that the twitch tension of the skeletal muscle decrease with a decrease in intracellular K+. The muscle tension also decreases with an increase in the ratio of intracellular and extracellular H+ concentration. However, there is no consistent relationship between muscle tension and extracellular or intracellular pH. The muscle tension of the diaphragms taken from K+-deficient rats is more sensitive to variations in CO2, PH, and bicarbonate concentration of the medium than that of the control rat diaphragms.

Acid-Base Equilibrium↗
PubMed1983

Endogenously synthesized prostaglandins stimulate sympathetic nervous system activity.

We examined the effect of an increase of endogenous prostaglandin production, induced by potassium depletion, on the urinary excretion of the norepinephrine metabolites metanephrine, normetanephrine and MHPG. Potassium deficiency caused a significant increase in all three metabolites. Treatment with indomethacin, 10 mg/day for 5 days, partially reversed the increase in the urinary excretion of norepinephrine metabolites. These findings suggest that in the intact organism prostaglandins stimulate, rather than inhibit norepinephrine release. Stimulation of prostaglandin synthesis may lead to an increase in sympathetic nervous system activity by a direct action or via a baroreceptor feedback mechanism.

Animals↗
PubMed1997

Potassium depletion and acid-base transporters in rat kidney: differential effect of hypophysectomy.

Potassium depletion is involved in the pathophysiology of metabolic alkalosis. In the present study, the expression of renal acid-base transporters that are involved in HCO3- reabsorption was studied in potassium depletion. Rats fed potassium-deficient (KD) diet developed significant hypokalemia at 14 days (serum K+ 1.9 +/- 0.2 in KD vs. 4.2 +/- 0.2 meq/l in control, P < 0.01) but not at 6 days (3.8 +/- 0.3 in KD vs. 4.1 +/- 0.3 meq/l in control, P > 0.05). Kidney mRNA for colonic H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase, cHKA) increased by approximately 3- and 11-fold at 6 and 14 days of KD diet, respectively, indicating that increased expression preceded the onset of hypokalemia. The expression of Na+/H+ exchanger 3 (NHE-3) mRNA and its cognate protein remained unchanged at 6 and 14 days of KD diet. The mRNA levels for NHE-1, NHE-2, and NHE-4 also remained unchanged at 6 and 14 days of KD diet. Hypophysectomized (HPX) rats fed KD diet for 14 days developed similar hypokalemia. However, the expression of cHKA mRNA in the kidney was decreased by approximately 80% in potassium-depleted (HPX+KD) rats (P < 0.01 vs. KD only). Hypophysectomy did not affect the mRNA levels for either gastric H(+)-K(+)-ATPase (gHKA) or NHE isoforms in KD animals. Thus potassium depletion increases expression of cHKA in the kidney but not that of gHKA or NHE isoforms. The signal for this increase appears to precede hypokalemia. Furthermore, the data suggest that pituitary hormone(s) plays an important and novel role in the regulation of cHKA.

Acids↗
PubMed1981

Cardiac arrhythmias in space. Role of vagotonia.

Rhythm disorders observed in space have always been minor but they are not unfrequent. They include: ventricular or supra-ventricular extrasystoles, nodal arrhythmias, auriculo-ventricular conduction disorders. There are several etiopathogenetic hypotheses: a strict selection must permit its elimination of an underlying heart disease; the potassium deficiency is often advanced but its role is not certain; the role of catecholamines is also discussed; the role of hypervagotony is extensively analysed as great clinical and electro-cardiographic evidence speaks for it. It can induce disorders which are more serious than those observed so far, particularly fibrillation or intermittent atrial flutter; weightlessness itself could partly condition the vagotonic state; and the effects of fluid shifts are also discussed from this point of view. The possible therapies for various atrial, nodal, ventricular disorders are reviewed, with greater detail for vagal atrial arrhythmias.

Adaptation, Physiological↗
PubMed2005

Severe syncope and sudden death in children with inborn salt-losing hypokalaemic tubulopathies.

BACKGROUND: Potassium deficiency may cause cardiac arrhythmias culminating in syncope or sudden death. METHODS: An inquiry performed among physicians caring for a total of 249 patients with inborn salt-losing tubulopathies revealed that acute cardiac complications occurred in seven children. RESULTS: Four patients died suddenly and three had severe syncope. These episodes occurred in the context of severe chronic hypokalaemia (< or =2.5 mmol/l) or were precipitated by acute diseases, which exacerbated hypokalaemia (< or =2.0 mmol/l). CONCLUSIONS: In conclusion, severe chronic or acute hypokalaemia is hazardous in inborn salt-losing tubulopathies.

Child↗
PubMedDate not supplied

Effects of low-potassium diet on N-ethylmaleimide-sensitive ATPase in the distal nephron segments.

The present study was undertaken to investigate whether or not potassium deficiency influences N-ethylmaleimide (NEM)-sensitive ATPase in the distal nephron segments of the rat. One group of animals was fed a low-K diet, whereas the normal K-group was given the same diet after supplementation with KCl. The nephron segments examined were: the medullary and cortical thick ascending limbs, the distal convoluted tubule, and the cortical, outer and inner medullary collecting ducts. NEM-sensitive ATPase activity in microdissected segments was measured by a fluorometric microassay. The plasma K+ concentration in the low-K group was 3.1 +/- 0.3 mEq/l compared with 4.2 +/- 0.1 mEq/l in the normal-K group. NEM-sensitive ATPase activity in the outer medullary collecting duct of low-K diet animals was significantly greater than in normal-K animals. There was no significant difference in NEM-sensitive ATPase activity between the two groups of animals in the other nephron segments examined. It is suggested that NEM-sensitive H-ATPase activity in the outer medullary collecting duct is modulated by the potassium status of the animal.

Animals↗
PubMedDate not supplied

[Cardiovascular pathology and magnesium].

There is no univocal clinical cardiovascular pattern associated with magnesium deficiency. Only an acute hypomagnesaemia gives the evidence of a real magnesium deficiency. Arrhythmias corrected by magnesium are associated with potassium deficiency. Magnesium deficiency appears to be one risk factor of arrhythmias and coronary spasms. The influence of intravenous magnesium salts was clearly evaluated on cardiovascular electrophysiology allowing protocols infusion. The major beneficial effect of magnesium on total incidence of arrhythmias appears to have been due to a reduction in supraventricular tachyarrhythmias and especially in "torsade de pointes". Antiarrhythmic mechanisms still remain to be clarified. It is likely that magnesium influences cardiac conduction and refractoriness by affecting calcium dependent processes as if acting as an indirect inactivator of slow inward calcium current, probably secondary to an inward shift of the background potassium mediated current. Recent studies demonstrated beneficial effect of intravenous magnesium treatment in acute myocardial infraction, both as to mortality and to early cardiac insufficiency. Beside antiarrhythmic and vasodilatator effects, magnesium seems to show cardiac cells protective action against ischaemia.

Animals↗
PubMed1966

Hypertension, increased aldosterone secretion and low plasma renin activity relieved by dexamethasone.

A father and son are described with a condition characterized by benign hypertension, potassium deficiency, increased aldosterone secretion rate (ASR), raised plasma volume and suppressed plasma renin activity (PRA). There were intermittent elevations of urine 17-ketosteroids and 17-hydroxycorticoids (17-OHCS) but no increase in urine THS, normal circadian rhythm of plasma 17-OHCS, and normal urine 17-OHCS response to dexamethasone and intravenous ACTH. Plasma ACTH and corticosterone secretion were not elevated. Pregnanetriol excretion was normal but urine pregnanediol was increased. At operation on the father no adrenal tumour was found; the excised left adrenal weighed 7 g. and showed nodular cortical hyperplasia; juxtaglomerular cells showed only occasional granules. Following operation hypertension persisted and ASR was half the preoperative value. All abnormalities in father and son were relieved by dexamethasone (DM) 2 mg. daily. The condition recurred following cessation of DM but was relieved by a second course of treatment. No such response to DM was seen in a normal subject or in a patient with Conn's syndrome. For a number of reasons it is suggested that patients with hypertension, increased ASR and low PRA be given a trial of dexamethasone treatment before undergoing adrenal surgery.

17-Hydroxycorticosteroids↗
PubMed1976

Heat illness. II. Pathogenesis.

The effects of elevated temperatures and the time-temperature combinations for irreversible damage are outlined. Coagulation abnormalities and the effects on the kidney, liver, heart, brain and serum enzymes, the role of electrolytes and water, including salt deficiency and the controversial question of salt supplements, potassium deficiency, changes in other electrolytes and sweat solutes, and rhabdomyolysis (including a discussion of experimental work on dogs) are reviewed. The section ends with a discussion of the effects of drugs and an account of a recent fatal case of heat stroke which may have been triggered by chlorpromazine therapy.

Adolescent↗
PubMed1978

Collecting duct hydrogen ion secretion in the rabbit: role of potassium.

The purpose of this study was to investigate distal nephron hydrogen ion secretion in the intact animal. The rabbit was chosen as the experimental model because it produces acid urine containing little ammonium. Upon replacement of the usual rabbit diet with milk, plus administration of an acid load (10 mEq/kg), the urine pH fell consistently from very alkaline values (PH greater than 7.4) to 4.8 +/- 0.2. Despite the ability to achieve high urine-to-blood hydrogen ion concentration gradients, the U-B PCO2, an index of collecting duct hydrogen ion secretion, was virtually zero. In these studies, the urine bicarbonate and buffer concentration were comparable to those observed in dog, rat, and man in which a high U-B PCO2 gradient was achieved. The rabbits studied had low plasma potassium concentrations (less than 3 mEq/L). Since potassium deficiency has been implicated in impaired urine acidification, potassium was administered, and it resulted in an increase in collecting duct hydrogen ion secretion as evidenced by a further fall in minimum urine pH during acidemia and a prompt rise in the U-B PCO2 during alkali administration. In summary, rabbits had a very low but not absent rate of collecting duct hydrogen ion secretion. Potassium administration increased the rate of hydrogen ion secretion in a segment of the collecting duct in which hydrogen ion secretion is reflected by an increase U-B PCO2.

Acidosis↗