{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T03:19:31Z","timestamp":1790651971100,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,2,12]],"date-time":"2007-02-12T00:00:00Z","timestamp":1171238400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,2,15]]},"abstract":"<jats:p>Torsades de pointes (TdP) ventricular tachycardia typically occurs in the setting of early afterdepolarizations; it contributes to arrhythmias and sudden death in congenital and acquired heart disease. Window L\u2010type Ca<jats:sup>2+<\/jats:sup> current (<jats:italic>I<\/jats:italic><jats:sub>CaL<\/jats:sub>) has a central role in the arrhythmogenesis and may be particularly important under \u03b2\u2010adrenergic stimulation. We studied the properties of <jats:italic>I<\/jats:italic><jats:sub>CaL<\/jats:sub> in myocytes from the dog with chronic atrioventricular block (cAVB) that has cardiac hypertrophy and an increased susceptibility to TdP. Peak <jats:italic>I<\/jats:italic><jats:sub>CaL<\/jats:sub> densities at baseline (K<jats:sup>+<\/jats:sup>\u2010 and Na<jats:sup>+<\/jats:sup>\u2010free solutions, 10 mmol l<jats:sup>\u22121<\/jats:sup>[EGTA]<jats:sub>pip<\/jats:sub>) in cAVB were comparable to control, but inactivation was shifted to the right, resulting in a larger window current area in cAVB. Under \u03b2\u2010adrenergic stimulation, the window current area was increased and shifted to the left, but less so in cAVB (maximum at \u221227 mV, <jats:italic>versus<\/jats:italic>\u221232 mV in control). <jats:italic>I<\/jats:italic><jats:sub>CaL<\/jats:sub> during a step to \u221235 mV showed a transient reduction immediately after the peak. Test steps to 0 mV, simultaneous recording of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and manipulation of sarcoplasmic reticulum (SR) Ca<jats:sup>2+<\/jats:sup> release showed that this resulted from inhibition and fast recovery of <jats:italic>I<\/jats:italic><jats:sub>CaL<\/jats:sub> with SR Ca<jats:sup>2+<\/jats:sup> release. The extent of this dynamic modulation was larger in cAVB than in control (23 \u00b1 2% of the initially available current, <jats:italic>versus<\/jats:italic> 13 \u00b1 3%; <jats:italic>P<\/jats:italic> &lt; 0.05). Early afterdepolarizations (EADs) in cAVB myocytes under \u03b2\u2010adrenergic stimulation typically occurred in the window current voltage range and after decline of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. In conclusion, in cAVB, the larger window current, its rightward shift and enhanced dynamic modulation by SR Ca<jats:sup>2+<\/jats:sup> release may contribute to an increased incidence of EADs in cAVB under \u03b2\u2010adrenergic stimulation.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.124222","type":"journal-article","created":{"date-parts":[[2006,12,1]],"date-time":"2006-12-01T01:25:54Z","timestamp":1164936354000},"page":"147-160","source":"Crossref","is-referenced-by-count":58,"title":["Window Ca<sup>2+<\/sup> current and its modulation by Ca<sup>2+<\/sup> release in hypertrophied cardiac myocytes from dogs with chronic atrioventricular block"],"prefix":"10.1113","volume":"579","author":[{"given":"Gudrun","family":"Antoons","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul G. 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