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The slow force response to stretch: Controversy and contradictions
Author(s) -
Dowrick Jarrah M.,
Tran Kenneth,
Loiselle Denis S.,
Nielsen Poul M. F.,
Taberner Andrew J.,
Han JuneChiew,
Ward MarieLouise
Publication year - 2019
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.13250
Subject(s) - endoplasmic reticulum , extracellular , biophysics , mechanism (biology) , calcium , chemistry , intracellular , receptor , orai1 , neuroscience , microbiology and biotechnology , biology , physics , stim1 , biochemistry , organic chemistry , quantum mechanics
When exposed to an abrupt stretch, cardiac muscle exhibits biphasic active force enhancement. The initial, instantaneous, force enhancement is well explained by the Frank‐Starling mechanism. However, the cellular mechanisms associated with the second, slower phase remain contentious. This review explores hypotheses regarding this “slow force response” with the intention of clarifying some apparent contradictions in the literature. The review is partitioned into three sections. The first section considers pathways that modify the intracellular calcium handling to address the role of the sarcoplasmic reticulum in the mechanism underlying the slow force response. The second section focuses on extracellular calcium fluxes and explores the identity and contribution of the stretch‐activated, non‐specific, cation channels as well as signalling cascades associated with G‐protein coupled receptors. The final section introduces promising candidates for the mechanosensor(s) responsible for detecting the stretch perturbation.