In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 283, No. 4 ( 2002-10-01), p. H1515-H1522
Abstract:
An increase in coronary perfusion, transversal stretch of the myocardium, increases developed force (F dev ) (Gregg effect) through activation of stretch-activated ion channels (SACs). Lengthening of the muscle, longitudinal stretch of the myocardium, causes an immediate increase in F dev followed by a slow F dev 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 F dev and intracellular Ca 2+ concentration ([Ca 2+ ] i ) after a muscle length increase from 85% to 95% L max (length at which maximal isometric force develops) at low and high coronary perfusion before and after inhibition of SACs with gadolinium (10 μmol/l Gd 3+ ). The increase of F dev and peak [Ca 2+ ] i by the Gregg effect was of similar magnitude as the Anrep effect (from 3.5 ± 0.8 to 3.9 ± 1.2 mN/mm 2 and from 3.0 ± 0.7% to 3.8 ± 0.9% normalized [Ca 2+ ] i , means ± SE). SAC blockade completely blunted the increase of F dev and peak [Ca 2+ ] i by the Gregg effect; however, it did not affect the Anrep effect. The slow force response, but not the calcium response, was augmented by an increase in coronary perfusion. Therefore, increased coronary perfusion, transversal stretch of the myocardium, and muscle lengthening, longitudinal stretch of the myocardium, increase myocardial contraction in the rat through different stretch-triggered mechanisms.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.00113.2002
Language:
English
Publisher:
American Physiological Society
Publication Date:
2002
detail.hit.zdb_id:
1477308-9
SSG:
12
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