Abstract:
BACKGROUND:In large mammals and humans, the contribution of IKs to ventricular repolarization is still incompletely understood. METHODS AND RESULTS:In vivo and cellular electrophysiological experiments were conducted to study IKs in canine ventricular repolarization. In conscious dogs, administration of the selective IKs blocker HMR 1556 (3, 10, or 30 mg/kg PO) caused substantial dose-dependent QT prolongations with broad-based T waves. In isolated ventricular myocytes under baseline conditions, however, IKs block (chromanols HMR 1556 and 293B) did not significantly prolong action potential duration (APD) at fast or slow steady-state pacing rates. This was because of the limited activation of IKs in the voltage and time domains of the AP, although at seconds-long depolarizations, the current was substantial. Isoproterenol increased and accelerated IKs activation to promote APD95 shortening. This shortening was importantly reversed by HMR 1556 and 293B. Quantitatively similar effects were obtained in ventricular-tissue preparations. Finally, when cellular repolarization was impaired by IKr block, IKs block exaggerated repolarization instability with further prolongation of APD. CONCLUSIONS:Ventricular repolarization in conscious dogs is importantly dependent on IKs. IKs function becomes prominent during beta-adrenergic receptor stimulation, when it promotes AP shortening by increased activation, and during IKr block, when it limits repolarization instability by time-dependent activation. Unstimulated IKs does not contribute to cellular APD at baseline. These data highlight the importance of the synergism between an intact basal IKs and the sympathetic nervous system in vivo.
journal_name
Circulationjournal_title
Circulationauthors
Volders PG,Stengl M,van Opstal JM,Gerlach U,Spätjens RL,Beekman JD,Sipido KR,Vos MAdoi
10.1161/01.CIR.0000068344.54010.B3subject
Has Abstractpub_date
2003-06-03 00:00:00pages
2753-60issue
21eissn
0009-7322issn
1524-4539pii
01.CIR.0000068344.54010.B3journal_volume
107pub_type
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