Cytochalasin D alters kinetics of Ca2+ transient in rat ventricular cardiomyocytes: an effect of altered actin cytoskeleton?
The effects of cytochalasin D, a specific F-actin depolymerizing agent, on Ca2+ transients in rat ventricular cardiomyocytes were investigated. Cytochalasin D (20 microM) significantly slowed decay of Ca2+ transients (tau decay control cells=28.1+/-1.3, n=28tau decay=47.3+/-2.8 ms, n=20, P<0.001). The rising phase of Ca2+ transients was also significantly slower in cytochalasin D treated cells (tau rise=5.1+/-0.6 ms, n=17nu tau rise in control cells=3.6+/-0.2, n=21,P<0.01). Phalloidin (100 microM), an F-actin stabilizer, prevented cytochalasin D-induced alterations of Ca2+ transient kinetics. The cytochalasin D effect was not related to the l-type Ca2+ current since the current density and kinetics were not altered by the drug. We conclude that integrity of F-actin-based cytoskeleton is an important factor for sarcoplasmic reticulum function.
Undrovinas
A I
AI
Department of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, 2799 West Grand Boulevard, Detroit, MI, USA.
Maltsev
V A
VA
D000199:Actins / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D015638:Cytochalasin D / Q000494:pharmacology*; D003599:Cytoskeleton / Q000187:drug effects; D006352:Heart Ventricles / Q000166:cytology* / Q000378:metabolism*; D010590:Phalloidine / Q000494:pharmacology; D051381:Rats
D000199:Actins; D015220:Calcium Channels; D010590:Phalloidine; D015638:Cytochalasin D; D002118:Calcium