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See article by He et al. [1] (pages 298–307) in this issue. Congestive heart failure (CHF) is a complex syndrome that is the leading cause of death in Western society. A central feature of this syndrome is reduced cardiac contractility and blunted adrenergic responsiveness that together cause poor pump performance and limit exercise tolerance. Depression of myocyte contractility is thought to be a principle cause of the progressive decline in cardiac function that is a hallmark feature of end-stage CHF. The cellular and molecular basis of dysfunctional myocyte contractility in CHF is currently being studied in many laboratories in the hope that novel therapeutic targets can be identified. The manuscript by He et al. [1] in the current issue of Cardiovascular Research focuses on changes in transverse (T)-tubules and L-type Ca channel abundance in the contractile defects of ventricular myocytes from a canine model of CHF induced by rapid pacing.T-tubules are specialized invaginations of the surface membrane that serve to rapidly transmit the cardiac action potential deep into the core of large muscle cells, thereby producing synchronous contraction throughout the cell. L-type Ca channels are thought to be localized in high density within the T-tubules [2]. Depolarization of the T-tubules causes opening of L-type Ca channels [3], which elevates the [Ca] in the subsarcolemmal space where the T-tubules and the junctional sarcoplasmic reticulum (SR) are in close proximity. This elevation in subsarcolemmal Ca activates the calcium release channel (ryanodine receptor, RYR) to induce SR Ca release via calcium-induced calcium release (CICR) [4]). Reductions in the density of T-tubules and L-type Ca channels [1] should reduce the effectiveness of excitation-contraction coupling (ECC), slow the overall rate of SR Ca release and decrease the rate and magnitude of contraction.The cellular basis of contractile dysfunction in CHF is a … * Tel.: +1-215-707-3278; fax: +1-215-707-4003 srhouser{at}unix.temple.edu

Reduced abundance of transverse tubules and L-type calcium channels: another cause of defective contractility in failing ventricular myocytes