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Direct inhibition of cardiac L-type ...

Chen, Jianyong.

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Direct inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Direct inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids./
Author:	Chen, Jianyong.
Description:	163 p.
Notes:	Source: Dissertation Abstracts International, Volume: 62-03, Section: B, page: 1336.
Contained By:	Dissertation Abstracts International62-03B.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3007779
ISBN:	0493172165

Direct inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids.
Chen, Jianyong.

Direct inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids. - 163 p.

Source: Dissertation Abstracts International, Volume: 62-03, Section: B, page: 1336.

Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2001.

Cardiac L-type calcium channels play very important roles in cardiac functions. Under physiological conditions, they participate in the auto-depolarization of the cells in sinoatrial node, support the slow conduction of action potentials in atrio-ventricular node, and maintain the plateau of action potentials in atrial and ventricular cells. They initiate and control the strength of myocardial contraction, and play roles in the activation of cellular signaling pathways by controlling the influx of calcium ions. Under pathological conditions, such as during ischemia, the increased activity of the calcium channels is involved in arrhythmogenesis via accelerating pacemaker depolarizations, triggering afterdepolarizations, and promoting formation of reentry circuits. Therefore, maintaining the activity of the calcium channels at normal levels by regulators is crucial to prevent arrhythmogenesis. Thus, it is extremely important to understand the effects of channel regulators on the activity of the calcium channels during ischemia. One class of potential regulators of L-type calcium channels that has not been studied in detail are epoxyeicosatrienoic acids (EETs), which are produced by the metabolism of arachidonic acid in ischemic muscle. In order to characterize the effects of EETs on the activity of L-type calcium channels, channels were reconstituted in planar lipid bilayer or expressed in Xenopus oocytes so that the changes in the activity of L-type calcium channels during the application of EETs could be evaluated in detail. In this study, I found that EETs, at a concentration range of 10--100 nM, decreased the open probability, accelerated the inactivation rate, and reduced the unitary conductance of the calcium channels. These inhibitory effects of EETs are probably mediated by direct interaction between the calcium channels and EETs because EETs restricted in the lipid membrane were still able to exert their effects. Furthermore, alpha1C subunit of these calcium channels has been shown to be the major subunit for interaction with EETs because EETs had a significant inhibitory effects on alpha1C alone expressed in oocytes. Based on our knowledge of cardiac electrophysiology and cell biology, these direct inhibitory effects of EETs are beneficial for survival and functions of cardiac myocytes during ischemia.

ISBN: 0493172165Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Direct inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids.
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245 1 0 $a Direct inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids.
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500 $a Source: Dissertation Abstracts International, Volume: 62-03, Section: B, page: 1336.
500 $a Adviser: Robert L. Rosenberg.
502 $a Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2001.
520 $a Cardiac L-type calcium channels play very important roles in cardiac functions. Under physiological conditions, they participate in the auto-depolarization of the cells in sinoatrial node, support the slow conduction of action potentials in atrio-ventricular node, and maintain the plateau of action potentials in atrial and ventricular cells. They initiate and control the strength of myocardial contraction, and play roles in the activation of cellular signaling pathways by controlling the influx of calcium ions. Under pathological conditions, such as during ischemia, the increased activity of the calcium channels is involved in arrhythmogenesis via accelerating pacemaker depolarizations, triggering afterdepolarizations, and promoting formation of reentry circuits. Therefore, maintaining the activity of the calcium channels at normal levels by regulators is crucial to prevent arrhythmogenesis. Thus, it is extremely important to understand the effects of channel regulators on the activity of the calcium channels during ischemia. One class of potential regulators of L-type calcium channels that has not been studied in detail are epoxyeicosatrienoic acids (EETs), which are produced by the metabolism of arachidonic acid in ischemic muscle. In order to characterize the effects of EETs on the activity of L-type calcium channels, channels were reconstituted in planar lipid bilayer or expressed in Xenopus oocytes so that the changes in the activity of L-type calcium channels during the application of EETs could be evaluated in detail. In this study, I found that EETs, at a concentration range of 10--100 nM, decreased the open probability, accelerated the inactivation rate, and reduced the unitary conductance of the calcium channels. These inhibitory effects of EETs are probably mediated by direct interaction between the calcium channels and EETs because EETs restricted in the lipid membrane were still able to exert their effects. Furthermore, alpha1C subunit of these calcium channels has been shown to be the major subunit for interaction with EETs because EETs had a significant inhibitory effects on alpha1C alone expressed in oocytes. Based on our knowledge of cardiac electrophysiology and cell biology, these direct inhibitory effects of EETs are beneficial for survival and functions of cardiac myocytes during ischemia.
590 $a School code: 0153.
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