Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells.

Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Research Abstract Details 

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Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Abstract Text:

Shinya Kishida,Toshiaki Nakajima,Ji Ma,Taisuke Jo,Hiroyuki Imuta,Hitoshi Oonuma,Haruko Iida,Haruhito Takano,Toshihiro Morita,Ryozo Nagai,Shinya Kishida,Toshiaki Nakajima,Ji Ma,Taisuke Jo,Hiroyuki Imuta,Hitoshi Oonuma,Haruko Iida,Haruhito Takano,Toshihiro Morita,Ryozo Nagai,

Amiodarone (AM) is a potent vasodilator and exhibits diverse cardiovascular protective effects in vivo, but their underlying mechanisms remain unsettled. We investigated the effects of AM and N-desethylamiodarone (DEA), the major metabolite of AM, on endothelial nitric oxide (NO) production using cultured human umbilical vein endothelial cells (HUVECs). The release of NO was evaluated as measured by nitrite, a stable metabolite of NO, using the Griess reaction and also measured directly by a NO-selective electrode. The expression of each nitric oxide synthase (NOS) mRNA was examined by reverse transcriptase-polymerase chain reaction (RT-PCR), and the effects of AM on eNOS mRNA expression were studied by quantitative real-time RT-PCR. AM and DEA (1-30 microM) enhanced NO production in a concentration-dependent manner. DEA was capable of producing more NO than AM. L-NAME, a nonselective NOS inhibitor, EGTA, a Ca(2+)-chelating agent, and nickel, a nonspecific Ca(2+) blocker, all inhibited AM-induced NO production. However, LY294002, an Akt pathway inhibitor and SB202190, a MAP kinase inhibitor, did not significantly suppress the production. In RT-PCR analysis, only eNOS mRNA was detected. Treatment with AM for 4 hours did not show a significant increase in the expression of eNOS mRNA. AM lower than 30 microM did not induce apoptosis, net cell loss, or LDH release from cells. The present study provides the first evidence that therapeutic concentrations of AM and DEA enhance eNOS-mediated NO production without any toxic or apoptotic effects. This mechanism may underlie the cardiovascular protective effects of AM and its metabolite observed in a clinical setting.

Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Publishing Authors By Initials

S Kishida,T Nakajima,J Ma,T Jo,H Imuta,H Oonuma,H Iida,H Takano,T Morita,R Nagai,S Kishida,T Nakajima,J Ma,T Jo,H Imuta,H Oonuma,H Iida,H Takano,T Morita,R Nagai,

For similar chemical actions and uses: pharmacologic actions: therapeutic uses: cardiovascular agents: vasodilator agents research abstracts see: chemical actions and uses: pharmacologic actions: therapeutic uses: cardiovascular agents: vasodilator agents research

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Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: International heart journal

VOLUME: 47

Page Numbers: 85-93

Journal Abbreviation:

ISSN: 1349-2365

DAY: 13

MONTH: Jan

YEAR: 2006

Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Information

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LANGUAGE: eng

NlmUniqueID: 101244240

Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Keywords Mesh Terms:

KEYWORDS: Vasodilator Agents

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells. Information

Substance Name: Nitric Oxide Synthase

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Amiodarone and N-desethylamiodarone enhance endothelial nitric oxide production in human endothelial cells.

AFFILIATION: Department of Cardiovascular Medicine, University of Tokyo, Tokyo, Japan.

Country: Japan

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MEDLINETA: Int Heart J

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