Key result
In ferret ventricular muscle, 2,3-Butanedione monoxime (BDM) at 10 mM decreased peak tension to <10% of control and abolished the extra-light signal of aequorin in response to quick release.
Why the study?
Does 2,3-butanedione monoxime (BDM) alter the length-dependent intracellular Ca2+ transients in ferret ventricular muscle?
Does 2,3-butanedione monoxime (BDM) alter the length-dependent intracellular Ca2+ transients in ferret ventricular muscle?
The extra-light signal observed during quick release is tension-dependent, suggesting that tension reduction decreases the affinity of troponin-C for Ca2+ without altering the intact cardiac muscle Ca2+ handling system.
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Extra-light signals on quick release are BDM-sensitive; hypothesis-generating for mechanosensitive calcium handling but leaves open clinical relevance.
Kurihara et al. (1990) studied Ferret ventricular muscle. 2,3-Butanedione monoxime (BDM) vs. Control (absence of BDM) was evaluated on Intracellular Ca2+ transients (extra-light signal of aequorin) and peak tension. In ferret ventricular muscle, 2,3-Butanedione monoxime (BDM) at 10 mM decreased peak tension to <10% of control and abolished the extra-light signal of aequorin in response to quick release.
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