Abstract
AbstractActomyosin from crayfish skeletal muscle will superprecipitate in the presence of ATP without added Ca++ or Mg++. EDTA totally inhibits Ca++‐induced superprecipitation of actomyosin, but in some cases Mg++ will reverse this effect. It is suggested that Mg++ and not Ca++ is a prerequisite for superprecipitation with ATP alone. EDTA only partly inhibits heavy metal‐induced actomyosin superprecipitation.Heavy metal cations induce far greater actomyosin superprecipitation than Ca++, and they can even enhance previously formed Ca++‐induced precipitates. It is suggested that heavy metal cations may be more strongly bound to crayfish actomyosin than Ca++, and that they may displace Ca++ from existing actomyosin binding sites. Heavy metal potentiation of muscular contraction may thus involve direct action at myofibril binding sites.Caffeine and quinine are without effect either on the rate or extent of development of actomyosin precipitates in the presence of ATP, ATP plus Ca++, and ATP plus Zn++. These observations rule out any direct effect of these drugs at the myofibril level during drug‐induced potentiation of muscular contraction.
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