Edward G. Lakatta

TL;DR: An important pathway for regulation of the betaAR by Ca(2+) channels is postulated, based on targeted expression of the L-VDCC alpha(1) subunit in transgenic mouse ventricles, which resulted in marked blunting of thebetaAR pathway.

TL;DR: An abnormal ST segment response to treadmill exercise has a low predictive value for future coronary events (angina pectoris, nonfatal myocardial infarction, or cardiac death) in apparently healthy individuals and the incidence of events was virtually identical between those with an initially abnormal response and those who converted from a normal to an abnormal response.

TL;DR: This review aims to integrate the traditional viewpoint that has emphasized the supremacy of the ensemble of surface membrane ion channels in spontaneous firing of the primary cardiac pacemaker, and these novel perspectives of cAMP-mediated PKA-dependent Ca(2+) cycling in regulation of the heart pacemaker clock, both in the basal state and during beta-adrenergic receptor stimulation.

TL;DR: The results emphasize the profound role of calcium in modulating cell oxygen consumption, energy balance, pH, excitability, and force production.

TL;DR: The mechanisms that generate pacemaking activity in human sinoatrial nodal cells are revealed and it is demonstrated that spontaneous rhythmic local Ca2+ releases were coupled to electrogenic surface membrane molecules to trigger rhythmic action potentials, and that Ca2–cAMP–protein kinase A (PKA) signaling regulated clock coupling.