Stretch-induced modifications of myocardial performance: from ventricular function to cellular and molecular mechanisms.
The purpose of this review is to give an integrative view of the effect of stretch on the myocardium from ventricular function changes to cellular and molecular mechanisms. The general approach will be to discuss the cellular and molecular events which can explain the findings obtained in the whole ventricle. Following the historical development, the classical analysis of the Starling mechanism and the basis of the length-dependent process are rapidly reviewed. We then analyze in greater detail the recent findings on the mechanisms of length-dependent activation changes in contractile protein affinity for calcium, changes in intracellular calcium release, action potential changes and stretch-activated ion channels and discuss the opposite effects of stretch on ventricular contraction (mainly deactivation shortening and viscoelastic properties of the myocardium). Besides the short-term contractile response to stretch, the longer-term effects of myocardial stretch which lead to ventricular hypertrophy will be also rapidly reviewed.
Crozatier
B
B
Unité INSERM U400, Faculté de Médecine, Creteil, France.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D003285:Contractile Proteins / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism; D016276:Ventricular Function / Q000502:physiology*
D003285:Contractile Proteins; D007473:Ion Channels; D011493:Protein Kinase C; D002118:Calcium