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Articles in PresS, published online ahead of print May 23, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00113.2002
Submitted on February 12, 2002
Accepted on May 20, 2002
1 Laboratory for Physiology, Institute for Cardiovasculair Research, VUMC, Amsterdam, The Netherlands
2 University of Antwerp, Department of Physiology and Medicine, Antwerp, Belgium
* To whom correspondence should be addressed. E-mail: lamberts{at}physiol.med.vu.nl.
An increase in coronary perfusion, transversal stretch of the myocardium, increases developed force (Fdev) (Gregg effect) through activation of stretch-activated ion channels (SACs). Lengthening of the muscle, longitudinal stretch of the myocardium, causes an immediate increase in Fdev followed by a slow Fdev increase (Anrep effect). In isometrically contracting perfused papillary muscles of Wistar rats we investigated whether both effects were based on similar stretch-induced mechanisms by measuring Fdev and intracellular Ca2+ ([Ca2+]i) following a muscle length increase from 85% to 95%Lmax at low and high coronary perfusion before and following inhibition of SACs with gadolinium (10 µmol/L, Gd3+). The increase of Fdev and peak [Ca2+]i by the Gregg effect was of similar magnitude as the Anrep effect (3.5±0.8 to 3.9±1.2 mN/mm2 and 3.0±0.7% to 3.8±0.9 % normalized [Ca2+]i, mean±SEM). SAC-blockade completely blunted the increase of Fdev and peak [Ca2+]i by the Gregg effect, however did not affect the Anrep effect. The slow force response, but not the calcium response, was augmented by an increase in coronary perfusion.Increased coronary perfusion, transversal stretch of the myocardium, and muscle lengthening, longitudinal stretch of the myocardium, increase myocardial contraction in rat through different stretch-triggered mechanisms.
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