The effects of thyroid hormones on3H-ouabain binding site concentration, Na, K-contents and86Rb-efflux in rat skeletal muscle

1986 ◽  
Vol 406 (5) ◽  
pp. 529-535 ◽  
Author(s):  
Keld Kjeldsen ◽  
Maria Elisabeth Everts ◽  
Torben Clausen
1986 ◽  
Vol 56 (3) ◽  
pp. 519-532 ◽  
Author(s):  
Keld Kjeldsen ◽  
Maria Elisabeth Everts ◽  
Torben Clausen

1. Using vanadate-facilitated [3H]ouabain binding, the effect of semi-starvation on the total concentration of [3H]ouabain-binding sites was determined in samples of rat skeletal muscle. When 12-week-old rats were semi-starved for 1, 2 or 3 weeks on one-third to half the normal daily energy intake, the [3H]ouabain-binding site concentration in soleus muscle was reduced by 19, 24 and 25% respectively. In extensor digitorum longus, diaphragm and gastrocnemius muscles the decrease after 2 weeks of semi-starvation was 15, 18 and 17% respectively. The decrease was fully reversible within 3 d of free access to the diet. Complete deprivation of food for 5 d caused a reduction of 25% in soleus muscle [3H]ouabain-binding-siteconcentration. It was excluded that the reduction in [3H]ouabain binding was due to a reduced affinity of the binding site for [3H]ouabain.2. Semi-starvation of 12-week-old rats for 3 weeks caused a reduction of 45 and 53% in 3, 5, 3'-triiodothyronine (T3) and thyroxine (T4) levels respectively. As reduced thyroid hormone levels have previously been found to decrease [3H]ouabain-binding-siteconcentration in skeletal muscle, this points to the importance of T3 and T4 in the down-regulation of the [3H]ouabain-binding-siteconcentration in skeletal muscle with semi-starvation. Whereas potassium depletion caused a decrease in K content as well as in [3H]ouabain-binding-siteconcentration in skeletal muscles, semi-starvation caused only a tendency to a decrease in K content. Thus, K depletion is not a major cause of the reduction in [3H]ouabain-binding-siteconcentration with semi-starvation.3. Due to its high concentration of Na, K pumps, skeletal muscle has a considerable capacity for clearing K from the plasma as well as for the binding of digitalis glycosides. Semi-starvation causes a severe reduction in the total skeletal muscle pool of Na, K pumps and may therefore be associated with impairment of K tolerance and increased digitalis toxicity.


1993 ◽  
Vol 75 (1) ◽  
pp. 173-180 ◽  
Author(s):  
M. J. McKenna ◽  
T. A. Schmidt ◽  
M. Hargreaves ◽  
L. Cameron ◽  
S. L. Skinner ◽  
...  

This study investigated the effects of sprint training on muscle Na(+)-K(+)-adenosinetriphosphatase (ATPase) concentration, plasma [K+] regulation, muscle performance, and fatigue during severe intermittent exercise. Six untrained male subjects underwent intensive cycle-sprint training for 7 wk. Muscle biopsies were taken at rest from the vastus lateralis muscle before and after 7 wk of training and were assayed for Na(+)-K(+)-ATPase concentration using vanadate-facilitated [3H]ouabain binding to intact samples. Before and after the training period, subjects performed four maximal 30-s exercise bouts (EB) on a cycle ergometer, each separated by a 4-min recovery. Arterialized venous blood samples were drawn immediately before and after each sprint bout and were analyzed for plasma [K+]. The work output was significantly elevated (11%) across all four EBs after training. The muscle [3H]ouabain binding site concentration was significantly increased (16%) from 333 +/- 19 to 387 +/- 15 (SE) pmol/g wet wt after training but was unchanged in muscle obtained from three control subjects. Plasma [K+] rose by 1–2 mmol/l with each EB and declined rapidly by the end of each recovery period. The increases in plasma [K+] resulting from each EB were significantly lower (19%) after training. The ratios of rise in plasma [K+] relative to work output during each EB were also significantly lower (27%) after training. The increased muscle [3H]ouabain binding site concentration and the reduced ratio of rise in [K+] relative to work output with exercise are both consistent with improved plasma and skeletal muscle K+ regulation after sprint training.


1997 ◽  
Vol 152 (1) ◽  
pp. 49-57 ◽  
Author(s):  
I Dørup ◽  
T Clausen

Abstract Since adrenal steroids have been shown to upregulate the concentration of Na+–K+-ATPase in cardiac muscle, similar effects could be expected in skeletal muscle. Following infusion of dexamethasone (0·02–0·1 mg/kg per day) for 7 days in 10-week-old rats, the total concentration of [3H]ouabain-binding sites rose by up to 22–42% in soleus, extensor digitorum longus, gastrocnemius and diaphragm muscle. Dexamethasone produced no or minute changes in the Na+–K+ contents of skeletal muscle. In contrast, infusion with aldosterone (0·02–0·5 mg/kg per day) for 7 days produced hypokalemia and a graded reduction in the K+ content of skeletal muscle, which was closely correlated to a downregulation of the [3 H]ouabain-binding site concentration (r= 0·65–0·70; P<0·001). The results indicate that in skeletal muscle high doses of glucocorticoids upregulate the concentration of Na+–K+ pumps whereas mineralocorticoids induce a downregulation, which is secondary to the concomitant K+ deficiency. Since adrenalectomy produced no significant change in [3 H]ouabain-binding site concentration, basal levels of endogenous adrenal steroids seem to be of minor importance for the regulation of Na+–K+ pump concentration in skeletal muscle. Journal of Endocrinology (1997) 152, 49–57


2017 ◽  
Vol 5 (7) ◽  
pp. e13219 ◽  
Author(s):  
Victoria L. Wyckelsma ◽  
Itamar Levinger ◽  
Robyn M. Murphy ◽  
Aaron C. Petersen ◽  
Ben D. Perry ◽  
...  

1986 ◽  
Vol 860 (3) ◽  
pp. 708-712 ◽  
Author(s):  
Keld Kjeldsen ◽  
Erik A. Richter ◽  
Henrik Galbo ◽  
Gilles Lortie ◽  
Torben Clausen

1988 ◽  
Vol 255 (5) ◽  
pp. E604-E612 ◽  
Author(s):  
M. E. Everts ◽  
T. Clausen

The effects of hypothyroidism and 3,5,3'-triiodothyronine (T3) treatment on passive Na+-K+ fluxes and Na+-K+ pump concentration were investigated in isolated rat muscle. Within 12 h after a single dose of T3 (20 micrograms/100 g body wt), K+ efflux had increased by 21% in soleus and by 20% in extensor digitorum longus muscle. In the presence of ouabain, even larger effects were observed. These changes were associated with a 12% rise in amiloride-suppressible Na+ influx but no significant increase in [3H]ouabain binding site concentration. After 3 days of T3 treatment, the stimulating effect on K+ efflux and Na+ influx in soleus reached a plateau approximately 80 and 40% above control levels, respectively, whereas the maximum increase in [3H]ouabain binding site concentration (103%) was only fully developed after 8 days. Hypothyroidism decreased 86Rb efflux by 30%. The efflux of K+ and the influx of Na+ per contraction (both approximately 7 nmol/g wet wt) as well as the net loss of K+ induced by electrical stimulation were unaffected by T3 treatment. The rise in resting K+ efflux after 12-24 h of T3 treatment could be partly blocked by dantrolene or trifluoroperazine, indicating that an increase in the cytoplasmic Ca2+ concentration may contribute to the early rise in K+ efflux. It is concluded that the early rise in the resting passive leaks of Na+ and K+ induced by T3 is a major driving force for Na+-K+ pump synthesis.


1997 ◽  
Vol 85 (4) ◽  
pp. 734-738 ◽  
Author(s):  
Kyung W. Park ◽  
Hai B. Dai ◽  
Kaie Ojamaa ◽  
Edward Lowenstein ◽  
Irwin Klein ◽  
...  

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