Origin of Mechanotransduction

Stretch-activated ion channels (SAC) serve as cardiac mechanotransducers. Mechanical stretch of intact tissue, isolated myocytes, or membrane patches rapidly elicits the opening of poorly selective cation, K+, and Cl− SAC. Several voltage- and ligand-gated channels also are mechanosensitive. SAC alter cardiac electrical activity and, with prolonged stretch, cause an intracellular accumulation of Ca2+ and Na+ that can serve to trigger multiple signaling cascades and ultimately may contribute to remodeling of the heart in response to hemodynamic stress. This chapter reviews the transmission of mechanical forces, the biophysical characteristics of cardiac SAC, and how SAC activity may be coupled to signaling cascades and thereby initiates the complex response of the heart to stretch.