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PubMed2006

(Borohydrido)(18-crown-6)potassium and (borohydrido)(dibenzo-18-crown-6)(tetrahydrofuran)potassium.

In the two compounds (borohydrido)(1,4,7,10,13,16-hexaoxacyclooctadecane-kappa(6)O)potassium, [K(BH(4))(C(12)H(24)O(6))], (I), and (borohydrido)(1,4,7,10,13,16-hexaoxa-2,3:11,12-dibenzocyclooctadeca-2,11-diene-kappa(6)O)(tetrahydrofuran)potassium, [K(BH(4))(C(4)H(8)O)(C(20)H(24)O(6))], (II), the K atom is bound to the six O atoms of the crown ether and to a tridentate borohydride group, with further coordination to a tetrahydrofuran molecule in (II). The alkali metal ion environment is thus distorted hexagonal-pyramidal in (I) and bipyramidal in (II).

Journal Article↗
PubMed2006

Efficacy and tolerability of diclofenac potassium sachets in acute postoperative dental pain: a placebo-controlled, randomised, comparative study vs. diclofenac potassium tablets.

This double-blind, randomised, parallel-group trial compared the analgesic efficacy of single 50 mg doses of diclofenac potassium sachets and tablets with placebo in 184 patients with moderate/severe pain after third molar extraction. The primary efficacy variable was the average pain reduction from baseline during the first 2-h postdose, using a visual analogue scale (VAS). During the first 2-h postdose, sachets and tablets significantly reduced pain (p < 0.05) vs. placebo with an incremental benefit seen for sachets over tablets (p < 0.05). Onset of analgesic effect (VAS) was at 30 min for sachets and 45 min for tablets. Pain reduction vs. placebo (VAS) was maintained for 8 h for sachets and tablets (p < 0.05). VAS-findings were confirmed by pain relief and intensity verbal scale assessments. Fewer patients re-medicated vs. placebo. No safety issues were identified. This study demonstrates that both diclofenac potassium sachets and tablets offer patients suffering from acute pain conditions an effective treatment with incremental analgesic benefits seen for sachets.

Adolescent↗
PubMed2005

Potassium deposition during and after hypokinesia in potassium supplemented and unsupplemented rats.

The aim of this study was to determine that hypokinesia (restricted motor activity) could increase potassium (K+) losses with decreased tissue K+ content showing decreased K+ deposition. To this end, measurements were made of K+absorption, tissue K+ content, plasma K+ levels, fecal and urinary K+ excretion during and after hypokinesia (HK) with and without K+ supplementation. Studies conducted on male Wistar rats during a pre-hypokinetic period, a hypokinetic period and a post-hypokinetic period. Rats were equally divided into four groups: unsupplemented vivarium control rats (UVCR), unsupplemented hypokinetic rats (UHKR), supplemented vivarium control rats (SVCR) and supplemented hypokinetic rats (SHKR). SHKR and UHKR were kept in small individual cages which restricted their movements in all directions without hindering food and water consumption. SVCR and UVCR were housed in individual cages under vivarium control conditions. SVCR and SHKR consume daily 3.96 mEq potassium chloride (KCl) per day. Absorption of K+, and K+ levels in bone, muscle, plasma, urine and feces and PA levels did not change in SVCR and UVCR compared with their pre-HK levels. During HK, plasma, fecal and urinary K+ levels and plasma aldosterone (PA) levels increased significantly (p<0.05) with time, while K+ absorption, muscle and bone K+ content decreased significantly (p<0.05) with time in SHKR and UHKR compared with their pre-HK values and the values in their respective vivarium controls (SVCR and UVCR). During the initial 9-days of post-HK, K+ absorption increased significantly (p<0.05) and plasma K+ levels, fecal and urinary K+ losses and PA levels decreased significantly (p<0.05) and muscle and bone K+ content remained significantly (p<0.05) depressed in SHKR and UHKR compared with their pre-HK and their respective vivarium control values. During HK and post-HK periods, K+ absorption, bone and muscle K+ content, and K+ levels in plasma, urine and feces and PA levels were affected significantly (p<0.05) more in SHKR than in UHKR. By the 15th day of post-HK the values in SHKR and UHKR approach the control values. The higher K+ losses during HK with decreased tissue K+ levels shows decreased K+ deposition. The higher K+ loss with lower tissue K+ levels in SHKR than in UHKR shows that K+ deposition decreases more with K+ supplementation than without. Because SHKR had shown lower tissue K+ content and lost higher K+ amounts than UHKR it was concluded that the risk of decreased K+ deposition and tissue K+ depletion is inversely related to K+ intake, i.e., the higher K+ intake, the greater the risk for decreased K+ deposition, and the higher K+ losses and the greater the risk for tissue K+ depletion. The dissociation between tissue K+ depletion and K+ excretion indicates decreased K+ deposition as the principal mechanism of tissue K+ depletion during prolonged HK.

Journal Article↗
PubMed1989

Comparison of effects of a potassium channel opener BRL34915, a specific potassium ionophore valinomycin and calcium channel blockers on endothelin-induced vascular contraction.

The effects of a potassium (K+) channel opener BRL34915 and a specific K+ ionophore valinomycin on vasoconstriction induced by endothelin (ET) were compared with those of calcium (Ca2+) channel blockers, nicardipine and verapamil, using helical strips from rat thoracic aorta. ET induced potent and persistent contraction in control solution and similar but smaller contraction in Ca2+-free solution. BRL34915 and valinomycin inhibited the ET-induced contraction dose-dependently in control solution, but not in Ca2+-free solution. The ET-induced contraction was also inhibited by nicardipine and verapamil, though less strongly. On the other hand, high K+ (35 mM)-induced vasoconstriction was strongly inhibited by nicardipine and verapamil, but not by BRL34915 or valinomycin. These results support the idea that the extracellular Ca2+-dependent component of the ET-induced contraction may be mediated by Ca2+ influx by a route other than voltage-dependent Ca2+-channels.

Animals↗
PubMed1991

Response of infant and adult rat choroid plexus potassium transporters to increased extracellular potassium.

The choroid plexus (CP) has an important role in regulating ion concentrations in the cerebrospinal fluid (CSF). Maintenance of potassium concentration [( K]) in brain extracellular fluids lower than in serum is critical to proper neuronal function. We studied K (86Rb) transport by the isolated, lateral CP from infant and mature rats to determine the nature and development of CSF [K] regulation. Comparison of transport characteristics in media with 3-11 mM [K] showed that the adult CP increased uptake in a stepwise fashion with each 2 mM increase in [K], up to a 90% increase with 9 mM [K] over control (3 mM [K]). In contrast, 3-day CP increased uptake in 5 mM, but could not increase K uptake further with higher [K]. One-week tissues showed an intermediate response. Kinetic analysis of the ouabain-inhibitable component suggested that the immature tissues may express a different isoform of the catalytic (alpha) subunit of the Na,K-ATPase. These data may explain the previously established inability of neonatal rats to regulate CSF [K] when serum [K] is elevated, and they indicate that active K transport by the CP cells plays an integral role in CSF [K] regulation.

Aging↗
PubMed1999

Overexpression of a Shaker-type potassium channel in mammalian central nervous system dysregulates native potassium channel gene expression.

The nervous system maintains a delicate balance between excitation and inhibition, partly through the complex interplay between voltage-gated sodium and potassium ion channels. Because K+ channel blockade or gene deletion causes hyperexcitability, it is generally assumed that increases in K+ channel gene expression should reduce neuronal network excitability. We have tested this hypothesis by creating a transgenic mouse that expresses a Shaker-type K+ channel gene. Paradoxically, we find that addition of the extra K+ channel gene results in a hyperexcitable rather than a hypoexcitable phenotype. The presence of the transgene leads to a complex deregulation of endogenous Shaker genes in the adult central nervous system as well as an increase in network excitability that includes spontaneous cortical spike and wave discharges and a lower threshold for epileptiform bursting in isolated hippocampal slices. These data suggest that an increase in K+ channel gene dosage leads to dysregulation of normal K+ channel gene expression, and it may underlie a mechanism contributing to the pathogenesis of human aneuploidies such as Down syndrome.

Animals↗
PubMed2003

Dietary potassium and laxatives as regulators of colonic potassium secretion in end-stage renal disease.

BACKGROUND: In end-stage renal disease (ESRD), colonic potassium (K+) secretion increases as renal K+ excretion declines. The nature of this adaptive process is poorly understood, but post-prandial increases in plasma K+ concentration may be a determining factor. In addition, even though colonic K+ secretion increases in ESRD, interdialytic hyperkalaemia is a serious problem in haemodialysis patients, which might be reduced by stimulating colonic K+ secretion still further using laxatives. METHODS: Plasma K+ concentrations were measured in the fasting state, and for 180 min after the oral administration of 30 mmol of K+ to nine control subjects and 16 normokalaemic patients with ESRD (eight "predialysis" patients and eight patients undergoing continuous ambulatory peritoneal dialysis (CAPD)). Plasma K+ concentrations were also monitored for 180 min in fasting controls and ESRD patients who were not given the oral K+ load. To study the effect of laxatives on interdialytic hyperkalaemia, plasma K+ concentrations were measured in eight control subjects and 13 haemodialysis patients before and during 2 weeks treatment with bisacodyl (a cAMP-mediated laxative) and in five haemodialysis patients before and during 2 weeks treatment with lactulose (an osmotic laxative). RESULTS: Oral K+ loading caused plasma K+ concentration to rise within the normal range (3.5-5.1 mmol/l) in control subjects, while significantly higher concentrations were achieved in the "predialysis" patients and sustained hyperkalaemia developed in the CAPD patients. Bisacodyl treatment had no effect on plasma K+ concentrations in control subjects, but significantly decreased the mean interdialytic plasma K+ concentration (from 5.9+/-0.2 to 5.5+/-0.2 mmol/l, P<0.0005) in haemodialysis patients, whereas plasma K+ concentration did not change during lactulose treatment. CONCLUSIONS: Higher plasma K+ concentrations after food may help to maintain K+ homeostasis in ESRD by enhancing colonic K+ secretion. Bisacodyl may be useful for reducing interdialytic hyperkalaemia in patients undergoing haemodialysis.

Adult↗
PubMed1993

Actions of pinacidil at a reduced potassium concentration: a direct cardiac effect possibly involving the ATP-dependent potassium channel.

We investigated the effects of the ATP-dependent K+ channel antagonist glyburide and the ATP-dependent K+ channel agonist pinacidil in a Langendorff-perfused rabbit isolated heart subjected to a period of global hypoxia. A class III antiarrhythmic drug, E-4031, also was studied in this model. These studies aimed to define the mechanism of action of putative profibrillatory actions of pinacidil and the mechanism for the antifibrillatory effect of the class III antiarrhythmic drug, E-4031, in the hypoxic heart. After stabilization and determination of baseline functional parameters under normoxic perfusion conditions (95% O2/5% CO2), hearts were subjected to global hypoxia by switching to a 95% N2/5% CO2 saturated perfusion medium for a period of 12 min. After the hypoxic period, normoxia was re-established by switching to the oxygen-carbon dioxide saturated buffer medium for a period of 40 min. The oxygen tension of the perfusion buffer was reduced from approximately 400 mm Hg to below 50 mm Hg during the hypoxic period. All hearts subjected to hypoxia had reduced function: the left ventricular developed pressure and +/- dP/dt were reduced significantly. Myocardial tissue ATP concentrations were reduced (> 50%) in hearts subjected to hypoxia. Under conditions of hypoxic/reoxygenation and in the presence of a low (2.5 mM) potassium concentration ([K+]0), pinacidil (1.25 microM) facilitated the induction of ventricular fibrillation (80% fibrillation in the presence of pinacidil vs. 20% in the absence of pinacidil). Glyburide (10 microM) and E-4031 (1 and 10 microM) significantly reduced the incidence of ventricular fibrillation associated with pinacidil (20% fibrillation in the presence of hypoxia, pinacidil, and glyburide or 10 microM E-4031). Opening of the ATP-dependent K+ channel by pinacidil under normoxia and low K+ also facilitated the induction of ventricular fibrillation (60% ventricular fibrillation). Pinacidil failed to induce ventricular fibrillation under either normoxic or conditions of hypoxic/reoxygenation when the [K+]0 was increased to 5.1 mM. The results of this study demonstrate that K+ channel activators facilitate the induction of ventricular fibrillation under both normoxic conditions and conditions of hypoxic/reoxygenation when the perfusion buffer K+ concentration is reduced.

Adenosine Triphosphate↗
PubMedDate not supplied

Effect of potassium, angiotensin II and ACTH on blood aldosterone and cortisol in sheep on different dietary potassium and sodium intakes.

The short term aldosterone response to manipulations of potassium (K), angiotensin II (AII) and ACTH were examined in sheep on a variety of chronic electrolyte regimes. Reduction in Na intake increased blood aldosterone to a greater extent on 100 mmol/day K than a K-free diet. Aldosterone increased in response to AII under conditions of chronic dietary Na restriction, in contrast to acute Na depletion. The effects of K, AII, and ACTH on aldosterone concentrations in sheep on varying intakes of Na and K are similar to that reported for other species.

Adrenocorticotropic Hormone↗
PubMed1999

Effects of potassium intake on potassium, sodium and fluid balance in exercising horses.

The aim of this study was to investigate the adaptation to an increased potassium (K+) intake in horses and to study whether the regulation of the post exercise K+, sodium (Na+) and fluid balances were altered by an increased K+ intake. Four Standardbred horses were fed 2 levels (4.1 and 5.4 mmol/kg bwt/day) of K+ for 17 days in a crossover design. The effects on K+, Na+ and fluid balance were studied both at rest and in response to 29 km exercise. K+, Na+ and fluid intakes and outputs were balanced within 24 h after a new diet had been introduced. Adaptation consisted primarily of an increased urinary K+ excretion, later followed by an increase in faecal excretion. The increased urinary K+ excretion was associated with an increased mass of urine (1.2-1.4 kg/day) compensated for by an increased water intake. The sweat Na+ concentration was increased on the highest K+ intake (from 123 +/- 5 mmol/l to 138 +/- 3 mmol/l) and the urinary Na+ excretion was lower post exercise on this diet. There were no differences in the magnitude of post exercise hypokalaemia between the diets, and plasma K+ concentration was still reduced 24 h post exercise even when the horses were fed the higher K+ diet. Adaptation to an increased K+ intake was rapid in these horses and consisted mainly of an increased urinary excretion. The response to exercise was unaltered by the increased K+ intake, except for an increased Na+ concentration in sweat.

Aldosterone↗
PubMed1986

Effect of potassium concentration and ouabain on the renal adaptation to potassium depletion in isolated perfused rat kidney.

Renal adaptation for potassium (K) conservation has been demonstrated in isolated perfused kidneys from rats within 3 days of K depletion and appears to be independent of aldosterone and sodium excretion. This study was designed to investigate whether the renal adaptation for K conservation is independent of ambient [K] and renal tissue levels of K and whether ouabain may have effects on K excretion, which are in contrast to the effects on K excretion in normal animals. In the first study, rats K depleted for 3 days received 2500 mu equiv. KCI intraperitoneally, while other K-depleted rats and a group of control diet animals received intraperitoneal H2O alone to determine whether simple restoration of K deficits would reverse the renal adaptation for K conservation. Intraperitoneal KCI increased plasma [K] and kidney tissue K significantly within 3 h in the K-repleted group compared with the K-depleted rats. Isolated Kidneys were perfused from the three groups of rats 3 h after intraperitoneal injection. Despite K repletion in vivo, perfused kidneys from the K-repleted group still had significantly decreased K excretion (1.28 +/- 0.085 mu equiv./min) compared with controls (2.05 +/- 0.291 mu equiv./min), and K excretion was still not different from the K-depleted group (0.57 +/- 0.134 mu equiv./min). However, fractional K excretion by the kidneys from K-repleted rats was increased above K-depleted kidneys (0.48 +/- 0.051 vs. 0.18 +/- 0.034, p less than 0.01). Despite the increased renal tissue K in K-repleted kidneys at the start of perfusion (285 +/- 5.1 vs. 257 +/- 5.4 mu equiv./g), by the end of the perfusion tissue K in perfused kidneys was identical in all three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1985

Effect of aldosterone on potassium excretion during potassium chloride infusion in sheep.

Experiments were performed on normal mature ewes to quantitate the effect of acute variations in aldosterone activity on renal K excretion. Six-hour clearance studies were performed on three sheep. Treatments were control (no infusion), infusion of KCl (140 meq in 2 h) alone or with superimposed infusions of aldosterone (20 micrograms/h), or infusion of aldosterone antagonist potassium canrenoate (100 mg/h). During KCl infusion there were simultaneous increases in plasma K, K excretion, and Na excretion. Aldosterone treatment diminished the increase in plasma K and in Na excretion but increased the rate of K excretion. Canrenoate had opposite effects. The rate of change of K excretion relative to the change in plasma K was 417 for aldosterone and 102 microeq/min per meq/l for canrenoate treatments, P less than 0.05. Before KCl infusion aldosterone decreased the rate of Na excretion and the salivary Na-to-K ratio but did not alter plasma K or K excretion. Aldosterone has a potent kaliuretic action in sheep when plasma K is elevated.

Aldosterone↗
PubMed2006

Measuring partial body potassium in the arm versus total body potassium.

Skeletal muscle (SM), the body's main structural support, has been implicated in metabolic, physiological, and disease processes in humans. Despite being the largest tissue in the human body, its assessment remains difficult and indirect. However, being metabolically active it contains over 50% of the total body potassium (TBK) pool. We present our preliminary results from a new system for measuring partial body K (PBK) that presently are limited to the arm yet provide a direct and specific measure of the SM. This uniquely specific quantification of the SM mass in the arm, which is shielded from the body during measurement, allows us to simplify the assumptions used in deriving the total SM, thereby possibly improving the modeling of the human body compartments. Preliminary results show that PBK measurements are consistent with those from the TBK previously obtained from the same subjects, thus offering a simpler alternative to computed tomography and magnetic resonance imaging used for the same purposes. The PBK system, which can be set up in a physician's office or bedside in a hospital, is completely passive, safe, and inexpensive; it can be used on immobilized patients, children, pregnant women, or other at-risk populations.

Adult↗
PubMed2003

MCC-134, a single pharmacophore, opens surface ATP-sensitive potassium channels, blocks mitochondrial ATP-sensitive potassium channels, and suppresses preconditioning.

BACKGROUND: MCC-134 (1-[4-(H-imidazol-1-yl)benzoyl]-N-methylcyclobutane-carbothioamide), a newly developed analog of aprikalim, opens surface smooth muscle-type ATP-sensitive potassium (K(ATP)) channels but inhibits pancreatic K(ATP) channels. However, the effects of MCC-134 on cardiac surface K(ATP) channels and mitochondrial K(ATP) (mitoK(ATP)) channels are unknown. A mixed agonist/blocker with differential effects on the two channel types would help to clarify the role of K(ATP) channels in cardioprotection. METHODS AND RESULTS: To index mitoK(ATP) channels, we measured mitochondrial flavoprotein fluorescence in rabbit ventricular myocytes. MCC-134 alone had little effect on basal flavoprotein fluorescence. However, MCC-134 inhibited diazoxide-induced flavoprotein oxidation in a dose-dependent manner (EC(50)=27 micro mol/L). When ATP was included in the pipette solution, MCC-134 slowly activated surface K(ATP) currents with some delay (>10 minutes). These results indicate that MCC-134 is a mitoK(ATP) channel inhibitor and a surface K(ATP) channel opener in native cardiac cells. In cell-pelleting ischemia assays, coapplication of MCC-134 with diazoxide abolished the cardioprotective effect of diazoxide, whereas MCC-134 alone did not alter cell death. These results were reproducible in both rabbit and mouse myocytes. MCC-134 also attenuated the effect of ischemic preconditioning against myocardial infarction in mice, consistent with the results of cell-pelleting ischemia assays. CONCLUSIONS: A single drug, MCC-134, opens surface K(ATP) channels but blocks mitoK(ATP) channels; the fact that this drug inhibits preconditioning reaffirms the primacy of mitoK(ATP) rather than surface K(ATP), channels in the mechanism of cardioprotection.

Adenosine Triphosphate↗
PubMed1989

Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase.

We examined the hypothesis that proton-potassium-activated adenosine triphosphatase (H-K-ATPase) mediates K absorption and acidification in the inner stripe of the outer medullary collecting duct (OMCDi). Rabbits were fed a low-K diet (0.55% K) for 7-14 d because we have demonstrated previously that this low-K diet stimulates K-absorptive flux by the OMCDi. Proton secretion was measured as net total CO2 flux (JTCO2) by microcalorimetry. After basal collections, either vehicle or an inhibitor of gastric H-K-ATPase, omeprazole (0.1 mM), was added to the perfusate during the second period. Addition of vehicle to the perfusate changed neither the transepithelial voltage (VT, in millivolts) nor the JTCO2. In contrast, the addition of omeprazole (0.1 mM) to the perfusate abolished JTCO2 (from 14.5 +/- 5.6 to -0.1 +/- 3.1 pmol.mm-1.min-1) without significantly affecting VT. In additional experiments, in 16 tubules there was significant net K absorption (JK) of 5.0 +/- 1.0 pmol.mm-1.min-1 during the basal period, which exceeded the rate of K absorption that could be attributed to a paracellular voltage-mediated pathway (JKP = 1.0 +/- 0.4 pmol.mm-1.min-1, P less than 0.01). Administration of vehicle did not significantly affect either VT or JK. However, omeprazole abolished JK (from 5.1 +/- 1.0 to 0.1 +/- 2.5 pmol.mm-1.min-1) without affecting VT or JNa. The present results demonstrate that the OMCDi possesses an active, omeprazole-sensitive acidification and K-absorptive mechanism. These findings are consistent with the presence of H-K-ATPase activity in this nephron segment.

Absorption↗
PubMed2006

Characteristics of urine sodium and potassium after oral ingestion of solutions containing sodium and potassium which is isotonic to the physiological saline--a quantitative study.

The effects of orally ingesting 500 mL of four kinds of test solutions that were isotonic to physiological saline (i.e., containing sodium (Na) and potassium (K) as chloride with Na/K molar ratios of 1, 2, 3 and 4) on urine flow, Na and K excretions from Japanese male students were investigated. The subjects assembled at the National Institute of Nutrition the day before the oral ingestions, which were conducted three times for each subject. They were permitted to eat freely until 8:00 pm, and then the intake of food and drinks except tap water was prohibited until 10:00 pm. After that, no food or drinks except the test solution used, were permitted to be ingested until the end of the final collection of urine. Subjects were woken up at 7:00 am the next morning, at which time they emptied their bladder. At 8:00 am, after sampling control urine before ingestion, they ingested 500 mL of water, the physiological saline or one of the test solutions. Urine was collected every 30 min for 4 h after ingestion. Urine flow was significantly higher for those who drank solutions Na/ K = 1 and 2 than those who drank the saline (paired-t test), but that for those who drank solutions Na/K = 3 and 4 was not significantly higher. For those who drank solution Na/ k=2, urine Na was significantly higher than that of those who drank the saline 30 to 60 min after ingestion. An increase in urine flow after K ingestion may be an essential factor for K-induced Na uresis.

Administration, Oral↗
PubMed1987

Potassium balance of the 5 to 8-week-old broiler exposed to constant heat or cycling high temperature stress and the effects of supplemental potassium chloride on body weight gain and feed efficiency.

Four experiments were conducted to study the impact of ambient temperature and relative humidity stress upon K excretion and the effects of KCl supplementation of broilers exposed to chronic heat and cycling temperature stress. Potassium excretion, corrected for K intake and body weight, increased by 633% as ambient temperature was elevated from a constant 24 C to a constant 35 C. Feed (.73% K) and drinking water (0% K) were supplemented with KCl so effects of KCl on live weight gain and feed efficiency could be evaluated. In a previous study at thermoneutral temperature, no benefit of supplemental KCl was observed whereas in this study a dietary level of 1.5 to 2% K in the form of KCl improved gain under conditions of chronic high ambient temperature stress. This equals about 1.8 to 2.3 g K per chick daily or about .24 to .3% of the drinking water.

Animals↗
PubMed2000

Potassium, sodium and magnesium contents in skeletal muscle of renal stone-formers: a study in an area of low potassium intake.

Skeletal muscles surgically obtained from the stone-former group (external oblique muscle; n = 202, 82 males & 120 females), control group I (external oblique muscle; n = 5, all males), control group II (rectus abdominis muscle; n = 23, all females) and control group III (quadriceps femoris muscle; n = 11, all males) were analyzed for potassium (K), sodium (Na) and magnesium (Mg) contents. Muscle samples were digested with 65 per cent HNO3 and determined for K, Na and Mg by an atomic absorption spectrophotometer. The results of analysis showed the mean K, Na and Mg (+/- S.D.) contents in mumol per one gram of fresh tissue of the stone-former group, control groups I, II and III were 73.5 +/- 16.6, 51.3 +/- 13.4 and 6.6 +/- 1.3, 77.5 +/- 3.9, 43.9 +/- 9.9 and 7.2 +/- 0.5, 83.8 +/- 27.5, 49.4 +/- 24.1 and 6.7 +/- 1.8 and 85.0 +/- 17.1, 48.5 +/- 12.1 and 6.8 +/- 1.3. Among these variables, only the K content of control group III was higher significantly (p < 0.05) than that of the stone-former group. In the stone-former group, regression analysis showed significant correlations between K and Mg contents (r = 0.856, p < 0.001) and K and Na contents (r = -0.325, p < 0.001). Due to no available data of the external oblique, we made a comparison of our results to the soleus type of skeletal muscle of normal subjects reported by Dorup et al and found that the external oblique muscle had lower mean contents of K and Mg but a higher Na content than those of the soleus. Our results were similar to the K and Mg depleted muscles obtained from the patients receiving long-term treatment with diuretic drugs. The results suggest that most of our subjects in both the stone-former and the 3 control groups were in a state of K and Mg depletion. The causes may be multifactorial, for instance low intake, high sweat loss and the existence of environmental inhibitor (s) for K transport like vanadium.

Adult↗