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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Previous reports of the effects of disuse induced by tetrodotoxin (TTX) have demonstrated alterations in muscle function suggesting changes in the quality of contractile proteins. 2. We extended these studies to the effects of TTX-induced disuse on the Ca2+ activation characteristics of myofibrillar ATPase of the rat gastrocnemius. 3. Atrophic responses were as previously reported (St-Pierre, D.M.M. and Gardiner P.F. (1985) Effect of disuse on mammalian fast-twitch muscle: joint fixation compared with neurally applied tetrodotoxin. Exp. Neurol. 90, 635-651; St-Pierre, D.M.M. et al. (1987). Recovery of muscle from tetrodotoxin-induced disuse and the influence of daily exercise; 1. Contractile properties. Exp. Neurol. 98, 472-488.) with a significant decrease in left gastrocnemius weight compared to control (C) (1.25 +/- 0.06 for C vs 0.72 +/- 0.04 for TTX, X +/- SEM, P less than or equal to 0.01). 4. Myofibrillar protein yield (mg/g wet weight) was also depressed (92.8 +/- 4.5 for C vs 70.3 +/- 3.7 for TTX; P less than or equal to 0.01). 5. Maximum ATPase of myofibrils (nmol Pi/mg/min) was decreased (441 +/- 28 for C vs 181 +/- 30 for TTX, P less than or equal to 0.01). 6. Furthermore, the Hill n which reflects the cooperative aspects of Ca2+ activation of the myofibrillar ATPase was depressed (1.58 +/- 0.07 for C vs 1.29 +/- 0.09 for TTX; P less than or equal to 0.01). 7. The results suggest that muscle perturbations resulting from disuse are partially related to changes in the myofibril.
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PMID:TTX-induced muscle disuse alters Ca2+ activation characteristics of myofibril ATPase. 168 95

Myocardial Na,K-ATPase concentration was quantified in 18 0-8-year-old human subjects by vanadate-facilitated 3H-ouabain binding to intact samples of the left ventricle of the heart obtained at autopsy. Within the first 6 months of life, the Na,K-ATPase concentration showed a rapid decrease. The mean value in the age range from birth to 6 months was 1.6 times the mean value obtained in the age range 6 months to 8 years. The mean values +/- SEM were 1,076 +/- 57 (n = 10) and 671 +/- 28 (n = 8) (p less than 0.001) pmol/g wet weight, respectively. The highest value [1,433 +/- 56 pmol/g wet weight (n = 5)] was found in a 3-month-old child and the lowest value [545 +/- 22 pmol/g wet weight (n = 5)] in an 8-year-old. Evaluation of 3H-ouabain-binding kinetics showed no age-dependent variations. The total amount of Na,K-ATPase found in the heart was approximately 30 and 80 nmol within the first 3 years of life and at 8 years, respectively. The age-dependent change in myocardial Na,K-ATPase concentration can be ascribed to variation in the ratio between the amount of Na,K-ATPase and muscle mass during development. Since myocardial Na,K-ATPase is the receptor for cardiac glycosides, the present results may in part explain the clinical observation that cardiac glycoside sensitivity and toxicity change in young age.
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PMID:Age-dependent change in myocardial cardiac glycoside receptor (Na,K-pump) concentration in children. 168 31

Epithelial cell height was measured in order to estimate the cell volume of dark cells from the ampullae of the semicircular canal of the gerbil. Under control conditions, addition of 10(-4) mol/l piretanide, 10(-5) mol/l 5-nitro-2(3-phenylpropylamino)-benzoic acid (NPPB), 5 mmol/l barium or 10(-3) mol/l quinidine had no significant effect on cell height. Addition of 10(-4) mol/l NPPB or 10(-3) mol/l ouabain led to a small significant decrease in cell height which was not reversible. Substitution of Na+ by N-methyl-D-glucamine or of Cl- by gluconate led to a significant and reversible reduction in cell height. Isotonic elevation of [K+] from 3.6 to 25 mmol/l in a PO4-buffered, HCO3-free solution led to an increase in cell height from 5.8 +/- 0.1 (SEM) to 8.7 +/- 0.2 microns (n = 62) during the first 40 s. During prolonged exposure to elevated [K+] (3-5 min; n = 19), some tissue samples underwent a regulatory volume decrease. K(+)-induced swelling was absent in both isotonic Cl(-)-free and isotonic Na(+)-free solutions and was inhibited by the loop diuretic piretanide (10(-5) and 10(-4) mol/l) or by the (Na+ + K+) ATPase inhibitor ouabain (10(-3) mol/l) or by 10(-4) mol/l NPPB. After the removal of ouabain or 10(-4) mol/l NPPB, K(+)-induced swelling under control conditions was enhanced and was less reversible as compared to control conditions before the experiment. K(+)-induced swelling was not altered by NPPB (10(-5) mol/l) or barium (5 mmol/l); however, barium slowed shrinking upon return of [K+] to control level. In the presence of 10(-3) mol/l quinidine, K(+)-induced swelling was enhanced and not reversible. These data suggest that dark cells from the semicircular canal possess an Na+2Cl-K+ cotransporter as a solute uptake mechanism and a solute efflux mechanism which is sensitive to barium and inhibited by quinidine.
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PMID:K(+)-induced swelling of vestibular dark cells is dependent on Na+ and Cl- and inhibited by piretanide. 169 72

The effect of digoxin antibody fragments (Fab) on clearance of specifically bound digoxin from its specific receptor (Na, K-ATPase) was studied in human heart left ventricle (LV) and vastus lateralis skeletal muscle (SK) samples obtained postmortem. Initially, [3H]digoxin was bound to samples at conditions giving high relative occupancy of receptor. Half-life (t1/2) for its net release from LV in buffer was 32.2, 6.7, and 0.9 h at 0 degrees, 30 degrees, and 37 degrees C, respectively. For SK, t1/2 was 5.4 h in buffer at 30 degrees C. Inhibition of rebinding of digoxin by addition of specific digoxin Fab (5 x 10(-7) M) or excess unlabeled digoxin (1 x 10(-4) M) to buffer at 30 degrees C increased net release rate for specifically bound digoxin 2.5- to 3.0-fold in heart and SK. [3H]Digoxin was also bound to samples at conditions giving low relative occupancy. Samples were subsequently washed in buffer containing 5 x 10(-7) M specific digoxin Fab for 16 h at 30 degrees C. This wash reduced occupancy of receptors by digoxin from 10 to 0.5% in LV and from 9 to 0.3% in SK, respectively. At variance with wash at 37 degrees C, this procedure allowed subsequent vanadate-facilitated complete quantification of Na,K-ATPase by [3H]ouabain binding; values were 378 +/- 13 and 370 +/- 12 pmol/g wet weight (p greater than 0.6) in LV and 309 +/- 19 and 315 +/- 16 pmol/g wet weight (p greater than 0.7) in SK with and without previous wash, respectively (mean +/- SEM, n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced clearance of specifically bound digoxin from human myocardial and skeletal muscle samples by specific digoxin antibody fragments: subsequent complete digitalis glycoside receptor (Na,K-ATPase) quantification. 171 37

A method is presented for the micro-scale isolation and characterization of erythrocyte membrane Ca(2+)-ATPase from small samples (7 mL) of whole human blood. Ca(2+)-ATPase isolated by this technique was more than 92% pure and showed calcium-activation characteristics similar to enzyme purified by standard macroscale procedures--viz maximal velocity of activation (VCA2+) = 15.5 +/- 1.2 mumol ATP hydrolysed/mg/min, and reciprocal of apparent affinity (KCa2+) = 0.73 +/- 0.15 microM free calcium (mean +/- SEM; n = 9). Using the isolation procedure described, purified Ca(2+)-ATPase could be prepared and assayed in a single working day. When the calcium-activation kinetics of cystic fibrosis erythrocyte membrane Ca(2+)-ATPase were reassessed using enzyme purified by this technique, VCa2+ and KCa2+ were not significantly different from normal values.
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PMID:Purification and analysis of erythrocyte membrane Ca(2+)-ATPase from small samples of patient blood: application to cystic fibrosis. 183 18

To characterize renal transport of Na+ in heart failure, urinary Na+ excretion (UNaV), aldosterone levels, and Na,K-ATPase activity in isolated nephron segments were determined in three groups: control rats, rats with heart failure and moderate sodium retention, and rats with heart failure and severe sodium retention. Heart failure was induced by a fistula between the aorta and vena cava. For the control group, UNaV was 0.66 +/- 0.04 (mean +/- SEM) mueq/min, and aldosterone was 18.4 +/- 3.5 ng%. Na,K-ATPase activity (in 10(-11) mol/mm/min) was 28.4 +/- 1.1 in the proximal convoluted tubule, 23.3 +/- 1.0 in the proximal straight tubule, 37.4 +/- 1.9 in the medullary thick ascending limb, 40.2 +/- 1.9 in the cortical thick ascending limb, 43.2 +/- 2.2 in the distal convoluted tubule, and 20.5 +/- 0.9 in the cortical collecting duct. For the group with moderate heart failure, UNaV was 0.35 +/- 0.02 (p less than 0.001 versus control), and aldosterone was 15.9 +/- 4.4 (p = NS versus control). Na,K-ATPase activity was unchanged in the proximal convoluted tubule, proximal straight tubule, medullary thick ascending limb, and cortical collecting duct, but it increased in the cortical thick ascending limb to 57.7 +/- 3.1 (p less than 0.001 versus control) and decreased in the distal convoluted tubule to 35.3 +/- 1.2 (p less than 0.005 versus control). For the group with severe heart failure, UNaV was 0.029 +/- 0.016 (p less than 0.001 versus control), and aldosterone was 186.0 +/- 14.8 (p less than 0.001 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na,K-ATPase in isolated nephron segments in rats with experimental heart failure. 184 57

The impact of low level lead exposure on human central nervous system function is a major public health concern. This study addresses the inhibition of the cation pump enzyme Na, K-ATPase by low level lead. Human brain tissue was obtained at autopsy and frozen until use. Brain homogenates were preincubated with PbCl2 for 20 min at 0 degrees C. Inhibition of K-paranitrophenylphosphatase (pNPPase), a measure of the dephosphorylation step of Na,K-ATPase, reached steady state within 10 min. K-pNPPase activity, expressed (mean +/- SEM) as a percentage of control (45.2 +/- 2.7 nmol/mg/min), fell to 96.3 +/- 0.9% at 0.25 uM [PbCl2] to 82.0 +/- 1.6% at 2.5 uM [PbCl2] in homogenates prepared from normal brain. Similar results were obtained with homogenates prepared from brains of patients with a history of alcohol abuse and of those with other miscellaneous conditions. Since the mean blood level of lead in the United States has ranged recently from 9.2 to 16.0 ug/dl (0.44 to 0.77 uM), these results indicate that current in vivo levels of lead exposure may impair important human brain function.
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PMID:Low level lead inhibits the human brain cation pump. 185 20

The exchange of intramitochondrial ATP (ATP(in)) for extramitochondrial ATP (ATP(out)) was measured by using 31P NMR spectroscopy over a range of temperatures in isolated rat liver mitochondria oxidizing glutamate and succinate in the presence of external ATP but no added ADP (state 4). The rate of this exchange is more than an order of magnitude faster than rates reported previously that were determined by using isotopic techniques in the presence of oligomycin, the potent ATPase inhibitor. Differences are ascribed in part to the low levels of matrix ATP present in oligomycin-treated mitochondria. The addition of oligomycin to mitochondrial suspensions decreases intramitochondrial ATP levels from 17 +/- 3 (SEM) nmol/mg of protein in state 4 to 1.51 +/- 0.1 nmol/mg of protein in the presence of inhibitor at 8 degrees C. Simultaneously, transporter flux falls from 960 +/- 55 nmol/min.mg to undetectable levels (less than 300 nmol/min.mg). Although transport rates are much faster when measured by saturation-transfer than by conventional isotopic methods, the enthalpy values obtained by determining the effect of temperature on flux are very similar to those reported in the past that were determined by using isotopic techniques. Intramitochondrial ATP content regulates the rate of the ATP(in)/ATP(out) exchange. At 18 degrees C, the concentration of internal ATP that produces half-maximal transport rate is 6.6 +/- 0.12 nmol/mg of mitochondrial protein. The relationship between substrate concentration and flux is sigmoidal and is 90% saturated at 11.3 +/- 0.18 nmol/mg of mitochondrial protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:31P NMR saturation-transfer study of the in situ kinetics of the mitochondrial adenine nucleotide translocase. 188 22

In 15 conscripts, venous plasma potassium was followed during exercise on a training bicycle before and after 10 weeks of moderate physical training and a putative relationship with skeletal muscle Na,K-ATPase was evaluated. Peak plasma potassium concentration obtained at exhaustion was 6.1 +/- 0.2 and 5.6 +/- 0.2 mmol l-1 (mean +/- SEM, n = 14, P less than 0.05) before and after training, respectively. Throughout the exercise period and within the first minutes of rest plasma potassium concentration was 0.2-0.5 mmol l-1 higher before than after training. Neither peak values nor peak rises in plasma potassium concentration before nor after training were correlated to the 3H-ouabain binding site (Na,K-ATPase) concentration in vastus lateralis muscle. The results indicate that net loss of potassium from the skeletal muscle pool during exercise is reduced after training, that the heart during exercise may be exposed to a smaller rise in plasma potassium concentration after training than before, and that moderate improvement of capacity to clear extracellular potassium during exercise may be due to increased activity of existing Na,K-pumps in resting skeletal muscle fibres. This may reduce muscle fatigue, increase physical performance and explain the paradoxical observation that, despite an increased catecholamine response, there is a reduced risk of cardiac events after training.
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PMID:Exercise-induced hyperkalaemia can be reduced in human subjects by moderate training without change in skeletal muscle Na,K-ATPase concentration. 196 26

Male Wistar rats were killed 1, 2, or 4 days after a single intraperitoneal injection of cisplatin (5 mg/kg). Functional renal indices, enzymatic activities, and morphological variables were studied. One day after the injection, the treated group showed an increase in the magnesium and phosphate fractional urinary excretion (FE) vs the control group (FE Mg = 5.2 +/- SEM 0.5% vs 13.0 +/- 1.7%; P less than 0.01; and FE P = 4.7 +/- 0.7% vs 14.0 +/- 1.9%; P less than 0.01). Two days after cisplatin administration, a decrease in creatinine clearance of treated animals was found, to 0.33 +/- 0.03 vs 0.51 +/- 0.03 ml/min; P less than 0.05. Na-K-ATPase and ouabain-insensitive ATPase activities were studied in the proximal convoluted tubule, the medullary thick ascending limb of the Henle's loop (mTAL), and the distal convoluted tubule. Only in mTAL one day after the cisplatin injection was there a decrease in Na-K-ATPase activity in the treated group vs controls (1103 +/- 145 vs 1734 +/- 189 pmol Pi/mm.h; P less than 0.05). Morphological studies showed a decrease in mTAL diameters on day 1, and an increase in proximal convoluted tuble diameters at day 2 of treated rats vs controls, at 27.8 +/- 0.6 vs 31.4 +/- 0.7 microns; P less than 0.05, and 50.4 +/- 1.2 vs 47.4 +/- 0.2 microns; P less than 0.05 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of acute cisplatin administration on renal ATPase activities and magnesium excretion of rats. 196 57


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