Key result
Revisiting studies on calcium dependency of ATPase and tension under diastolic stretch reveals that the mechanisms of the Frank-Starling Law and hypertrophic myopathy are different.
Why the study?
Studies on Ca2+ dependency of ATPase and tension under diastolic stretch were revisited to re-evaluate conclusions on Hill coefficients.
This theoretical review suggests that the Frank-Starling Law and hypertrophic cardiomyopathy operate via different mechanisms, with the former being kinase-controlled.
Mechanisms of Frank-Starling Law and hypertrophic myopathy differ; leaves open kinase-targeted therapies pending prospective validation.
I have recently reiterated that the cross-bridge is a calcium ATPase that is inhibited by magnesium and this arises because in normal hearts Myosin binding Protein-C prevents the use of MgATP as rate limiting substrate ensuring that Ca2+ replaces Mg2+ in the excitation pathway. Here I revisit the studies on [Ca2+] dependency of ATPase and tension under diastolic stretch with a different conclusion on Hill coefficients. This reveals the underlying mechanisms of the Frank-Starling Law and Hypertrophic myopathy are not the same, the former being kinase controlled.
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Gerry A. Smith (2019) conducted a review in Familial Cardiomyopathy. Revisiting studies on calcium dependency of ATPase and tension under diastolic stretch reveals that the mechanisms of the Frank-Starling Law and hypertrophic myopathy are different.
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