Ca2+ currents in compensated hypertrophy and heart failure

摘要: Transmembrane voltage-gated Ca2+ channels play a central role in the development and control of heart contractility which is modulated by concentration free cytosolic calcium ions (Ca2+). are closed at normal membrane resting potential cardiac cells. During fast upstroke action (AP), they gated into an open state depolarisation thereby transduce electrical signal chemical signal. In addition to its contribution AP plateau, influx through L-type induces release from sarcoplasmic reticulum (SR) initiates contraction. Because their excitation-contraction (E-C) coupling, key target regulate inotropy [1]. The T-type more obscure. putative part rhythmic activity heart, may be implicated early stages during pathology contractile tissues [2]. Despite therapeutic advances improving exercise tolerance survival, congestive failure (HF) remains major problem cardiovascular medicine. It highly lethal disease; half mortality being related ventricular whereas sudden death other patients unexpected [3]. Although HF has diverse aetiologies, common abnormalities include hypertrophy, dysfunction alteration electrophysiological properties contributing low output death. A significant prolongation duration with delayed repolarisation been observed both compensated hypertrophy (CH) end-stage caused dilated cardiomyopathy (Fig. 1A) [4-8]. This lengthening can result either increase inward currents or decrease outward both. reduction K+ demonstrated [6,9]. Prolonged Na+/Ca2+ exchange current also involved [9]. contrast, there large variability results concerning (ICa). purpose this paper review obtained various animal models CH special emphasis on recent studies human We focus on: (i) pathophysiological channels, present some hypertrophy; (ii) density physiological regulations these rate beta-adrenergic receptor stimulation; (iii) molecular biology channel future directions.