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Received April 22, 2002
Accepted after revision July 1, 2002
1 Centre for Cardiovascular Biology and Medicine, Kings College London, St. Thomas's Campus, Lambeth Palace Road, London SE1 7EH, UK
* To whom correspondence should be addressed. E-mail: joanne.2.layland{at}kcl.ac.uk.
In cardiac muscle, B[%%%]-adrenergic stimulation increases contractile force and accelerates relaxation. The relaxant effect is thought to be due primarily to stimulation of Ca2+ uptake into the sarcoplasmic reticulum (SR), although changes in myofilament properties may also contribute. The present study investigated the contribution of the myofilaments to the B[%%%]-adrenergic response in isolated rat cardiac trabeculae undergoing either isometric or work-loop contractions (involving simultaneous force generation and shortening) at different stimulation frequencies (range 0.25-4.5 Hz). SR-dependent effects were eliminated by treatment with ryanodine (1 M[%%%]M) and cyclopiazonic acid (30 M[%%%]M). In isometric contractions during SR inhibition, isoprenaline increased the force but did not alter the time course of the twitch. In contrast, in work-loop contractions, the positive inotropic effect was accompanied by a reduced diastolic force between beats, most apparent at higher frequencies (e.g. diastolic stress fell from 58.6 ± 5.5 to 28.8 ± 5.8 mN mm-2 at 1.5 Hz). This relaxant effect contributed to a B[%%%]-adrenoceptor-mediated increase in net work and power output at higher frequencies, by reducing the amount of work required to re-lengthen the muscle. Consequently, the frequency for maximum power output increased from 1.1 ± 0.1 to 1.6 ± 0.1 Hz. We conclude that the contribution of myofilament properties to the relaxant effect of B[%%%]-stimulation may be of greater significance when force and length are changing simultaneously (as occurs in the heart) than during force development under isometric conditions.
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