LAUSR

Cardiac contraction is controlled by a Ca2+ signaling sequence that includes L-type Ca2+ current-gated opening of Ca2+ release channels (ryanodine receptors) in the sarcoplasmic reticulum (SR). Local Ca2+ signaling in the atrium differs from that in the ventricle because atrial myocytes lack transverse tubules and have more abundant corbular SR. Myocardium is subjected to a variety of forces with each contraction, such as stretch, shear stress, and afterload, and adapts to those mechanical stresses. These mechanical stimuli increase in heart failure, hypertension, and valvular heart diseases that are clinically implicated in atrial fibrillation and stroke. In the present review, we describe distinct responses of atrial and ventricular myocytes to shear stress and compare them with other mechanical responses in the context of local and global Ca2+ signaling and ion channel regulation. Recent evidence suggests that shear mechanotransduction in cardiac myocytes involves activation of gap junction hemichannels, purinergic signaling, and generation of mitochondrial reactive oxygen species. Significant alterations in Ca2+ signaling and ionic currents by shear stress may be implicated in the pathogenesis of cardiac arrhythmia and failure.