Circulation Research. 2001;88:1028-1035
Published online before print May 10, 2001, doi: 10.1161/hh1001.090876
Published online before print May 10, 2001, doi: 10.1161/hh1001.090876
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© 2001 American Heart Association, Inc.
Cellular Biology |
Titin-Based Modulation of Calcium Sensitivity of Active Tension in Mouse Skinned Cardiac Myocytes
From the Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology (O.C., Y.W., H.G.), Washington State University, Pullman, Wash, and the Center for Synchrotron Radiation Research and Instrumentation and Department of Biological, Chemical, and Physical Sciences (T.C.I.), Illinois Institute of Technology, Chicago, Ill. Present address of O.C. is INSERM U390/IFR3, Physiopathologie Cardiovasculaire, Montpellier, France.
Correspondence to Dr Henk Granzier, Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Wegner Hall, 205, Pullman, WA 88164. E-mail granzier{at}wsunix.wsu.edu
Abstract—We
studied the effect of titin-based passive force on the length
dependence of activation of cardiac myocytes to explore whether titin
may play a role in the generation of systolic force. Force-pCa
relations were measured at sarcomere lengths (SLs) of 2.0 and 2.3 µm.
Passive tension at 2.3 µm SL was varied from 
1 to 10
mN/mm2 by adjusting the characteristics of
the stretch imposed on the passive cell before activation. Relative to
2.0 µm SL, the force-pCa curve at 2.3 µm SL and low passive tension
showed a leftward shift (
pCa50 [change in
pCa at half-maximal activation]) of 0.09±0.02 pCa units while
at 2.3 µm SL and high passive tension the shift was increased to
0.25±0.03 pCa units. Passive tension also increased
pCa50 at reduced interfilament lattice
spacing achieved with dextran. We tested whether titin-based passive
tension influences the interfilament lattice spacing by measuring the
width of the myocyte and by using small-angle x-ray diffraction of
mouse left ventricular wall muscle. Cell width and
interfilament lattice spacing varied inversely with passive tension, in
the presence and absence of dextran. The passive tension effect on
length-dependent activation may therefore result from a radial
titin-based force that modulates the interfilament lattice
spacing.
Key Words: x-ray diffraction • myofilament lattice • collagen • Frank-Starling
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