Polymorphisms of the parkin gene in sporadic Parkinson's disease among Chinese in Taiwan

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Title:	Polymorphisms of the parkin gene in sporadic Parkinson's disease among Chinese in Taiwan
Authors:	Hu, CJ;Sung, SM;Liu, HC;Lee, CC;Tsai, CH;Chang, JG
Contributors:	附設醫院醫研部;China Med Coll Hosp, Dept Med Res, Div Mol Med, Taichung 400, Taiwan;Taipei City Psychiat Ctr, Taipei, Taiwan;Taipei Municipal Jen Ai Hosp, Dept Neurol, Taipei, Taiwan
Date:	2000
Issue Date:	2010-09-24 14:54:54 (UTC+8)
Publisher:	KARGER
Abstract:	The antiarrhythmic potential of acrophyllidine, a natural furoquinoline alkaloid isolated from the plant, Acronychia halophylla, has been documented. In the present study, the electrophysiological effects of acrophyllidine in Langendorff-perfused rat hearts and isolated cardiomyocytes were examined. In isolated rat heart (constant pressure), acrophyllidine suppressed ischemia/reperfusion-induced polymorphic ventricular tachyarrhythmias with an EC50 value of 4.4 mu M. In the perfused whole-heart model (constant flow), acrophyllidine increased the atrioventricular and His-Purkinje system conduction intervals, ventricular repolarization time (VRT), and basic cycle length and also prolonged the refractory periods of the AV node, His-Purkinje system and ventricle. In isolated rat ventricular myocytes, acrophyllidine prolonged the action potential duration (APD) and decreased both the maximal upstroke velocity of depolarization (V-max) and action potential amplitude in a concentration-dependent manner. Whole-cell voltage clamp studies show that acrophyllidine blocked the Na+ channel (IC50 = 3.6 mu M) With a negative-shift of its voltage-dependent steady-state inactivation curve and slowing of its recovery from inactivation. Similarly, Ca2+ inward current (I-Ca) was inhibited but to a lesser extent. Acrophyllidine also suppressed the transient outward (I-to) (IC50 equals; 4.5 mu M) and the steady-state outward K+ current (I-SS) (IC50 = 3.4 mu M) The inhibition of I-to was associated with an acceleration of its rate of inactivation. Additionally, acrophyllidine suppressed It, in a time-dependent manner and caused a negative-shift of the steady-state inactivation curve and a slowed rate of recovery from inactivation. It is concluded that acrophyllidine blocks Na-+,Na- I-to and I-SS channels and in similar concentrations partly blocks Ca2+ channel. These changes alter the electrophysiological properties of the conduction system and may be responsible for the termination of the ischaemia/reperfusion induced ventricular arrhythmias. (C) 2000 Wiley-Liss, Inc.
Relation:	EUROPEAN NEUROLOGY 44(2):90-93
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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