The slow increase in active stress following a step increase in cardiac muscle length in rabbits is independent of sarcoplasmic reticulum calcium content.
Challenges SR calcium dependence of length-mediated force in rabbits; leaves open translation to human cardiac adaptation or therapy.
After a step increase in length of rabbit right ventricular papillary muscles, active stress increased immediately followed by a further slow increase in stress over 15-20 min. We studied the contribution of the sarcoplasmic reticulum (SR) to the slow change in stress (SCS) after changing muscle length from 85 to 95% of length at which active force development was maximal. SCS amounted to 32.5 +/- 12.2% mean +/- SD, n = 19) of the total increase in active stress. This was associated with a 13.2 +/- 8.7% increase in calcium content of the SR as estimated with rapid cooling contractures (P < 0.0001, n = 19). However, SCS was not dependent on SR calcium content. There was no significant attenuation in SCS after SR calcium depletion with ryanodine (n = 6), SR Ca(2+)-adenosinetriphosphatase inhibition with cyclopiazonic acid (n = 6), or combined treatment with ryanodine and cyclopiazonic acid (n = 3). We conclude that, in the rabbit, SR calcium content increases slowly after a step increase in cardiac muscle length but the slow changes in active stress are not dependent on the sarcoplasmic reticulum.
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Bluhm et al. (1995) studied this question.
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