title: Heavy water effects on leaky heart muscle cells and actomyosin.
abstract: Heavy water inhibition of skeletal muscle contraction in barnacle and frog is thought to occur through inhibition of Ca release by SR. If this were so, D2O might be useful for studies on control of the inotropic state in mammalian myocardium. We therefore compared selected properties of mechanically disaggregated leaky myocardial fragments, and actomyosin, in D2O and H2O. At equal values of electrode-determined acidity the contraction frequency, initial velocity of 45Ca uptake, and equilibrium (Ca)i/(Ca)o of the myocardial fragments were all less when heavy water was used. For each of these parameters, and for actomyosin superprecipitation, the H2O and D2O acidity-response curves were similar but the D2O curve was shifted to the right. The actomyosin sedimentation rate was less in D2O than in H2O at near neutral acidity but not different under more acidic or basic conditions. Actomyosin ATPase showed an acidity-dependent increased activity in D2O. These results verify that heavy water inhibits contraction in mammalian myocardium, as is the case with invertebrate and frog skeletal muscle. The effect, however, cannot be attributed to inhibition of Ca release from SR.
mesh_terms: D000205:Actomyosin; D000255:Adenosine Triphosphate; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002384:Catalysis; D055598:Chemical Phenomena; D002621:Chemistry; D003864:Depression, Chemical; D003903:Deuterium / Q000494:pharmacology*; D004789:Enzyme Activation; D066298:In Vitro Techniques; D051379:Mice; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism
chemical_list: D000255:Adenosine Triphosphate; D000205:Actomyosin; D003903:Deuterium; D002118:Calcium