Editorials |
From the Department of Pharmacology (P.A.B.), Columbia University, New York, NY; and the Departments of Medicine, Physiology, and Biophysics (B.D.S., H.E.D.J.t.K.), University of Calgary, Calgary, Alberta, Canada.
Correspondence to Dr Penelope A. Boyden, Department of Pharmacology, Columbia College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032.
Key Words: Ca2+ waves Cai transients arrhythmias
| Introduction |
|---|
In the last 2 decades, a substantial body of literature documenting
Ca2+ waves in cardiac tissues has been created.
Studies on waves in cardiac cells provided fundamental information
about the role of the sarcoplasmic reticulum (SR) in
excitation-contraction coupling.2 Local contractions were
reported in cells with disrupted sarcolemma,2 clearly
demonstrating that Ca2+ waves were not related to
depolarization of the membrane. Interest in cardiac
Ca2+ waves was further stimulated by a study that
suggested a role for them in the generation of abnormal, nondriven
electrical activity of the heart.3 Initially,
Ca2+ waves in cardiac muscle were assessed
indirectly from observations of local sarcomere contraction and waves
of propagating sarcomere shortening,4 5 and direct
evidence
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