Editorials |
From the Molecular Physiology Section, Molecular Cardiology Laboratory, National Heart, Lung, and Blood Institute, Bethesda, Md.
Correspondence to Neal D. Epstein, MD, Molecular Physiology Section, Molecular Cardiology Laboratory, NHLBI, NIH, 10 Center Drive, MSC 1760, Building 10, Room 7B-15, Bethesda, MD 20892. E-mail epsteinn@mail.nih.gov
See related article, pages 12121218
Key Words: stretch-activation myosin kinetics cardiac regulatory light chain phosphorylation
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
You never know from where and when the next clue to any particular scientific problem will arise. In the case of cardiac function, it may have been in 1948 from Professor J.W.S. Pringle, who was trying to figure out how flies manage to fly upside down.1 Having mounted a truncated fly wing apparatus on a gyroscopic base, he serendipitously noted that when inertial and damping conditions were just right, the truncated wings oscillated at more than 100 s1 independent of neuronal innervation (Figure, A). This, he surmised, was attributable to matching an intrinsic resonant property of insect flight muscle to the elastic and inertial properties of the wing and exoskeletal structure, producing a resonant system generating oscillatory power. He called this intrinsic property of insect flight muscle "stretchactivation" because it is a recurrent stretching in the face of persistent Ca2+ levels, not Ca2+ pulses, that activate the actomyosin interaction in these insect flight muscles. This resonant system resembles a parent pushing a child on a swing. The parent must push at the correct time; that is, the addition of energy to the system must be matched to the intrinsic resonance of the system.
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Related Article:
Circ. Res. 2006 98: 1212-1218.
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