Effects of extracellular calcium concentration and dihydropyridines on contraction in mammalian skeletal muscle.

摘要: 1. Twitches, tetanic contractions and potassium contractures were recorded isometrically from small bundles of rat soleus muscle fibres. 2. Solutions with reduced calcium concentrations (low-calcium solutions), whether buffered EGTA (85 3 microM-Ca2+) or not (15 microM-Ca2+), caused an initial potentiation contraction followed by depression. 3. The decay (200 mM-potassium) was more rapid than normal in low-calcium solutions. 4. Recovery the inactivation produced a 200 mM-potassium contracture slowed solutions but full recovery seen within 10-15 min after return to solution containing 2.5 mM-Ca2+. 5. Nifedipine (50 microM) mM-Ca2+ potentiated whereas, solutions, depressed depression pronounced lower Ca2+ concentration. 6. As decayed rapidly nifedipine. still further rate 7. (-) Bay K 8644 contraction, increased inactivation, like racemate less effective. 8. In explanation these other observations, it is proposed that there dihydropyridine-binding molecule walls transverse tubular system normally exists predominantly 'precursor' form at resting membrane potential converted depolarization 'activator' essential for excitation-contraction coupling. Conversion precursor activator involves both conformational change dissociation calcium. Prolonged converts inactivated inducing requires reverse changes rebinding dihydropyridines affect reducing affinity