OXIDANTS AND NITRIC OXIDE IN CORONARY VASCULAR FUNCTION
冠状血管功能中的氧化剂和一氧化氮
基本信息
- 批准号:6316700
- 负责人:
- 金额:$ 39.44万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2000
- 资助国家:美国
- 起止时间:2000-07-01 至 2001-08-31
- 项目状态:已结题
- 来源:
- 关键词:animal tissue cellular respiration coronary artery enzyme activity exercise heart circulation heart failure heart metabolism heart pharmacology human tissue muscle metabolism nitric oxide nitric oxide synthase oxidative stress second messengers superoxide dismutase superoxides tissue /cell culture vascular endothelium vascular smooth muscle vasomotion
项目摘要
The long-range goals of this project are to develop an understanding of
the roles and mechanisms of action of oxidant and nitric oxide
interactions in vascular function in the coronary circulation and to
identify alterations that occur in these processes in the heart failure
and exercise training models examined in the Program Project. The first
objective is to determine mechanisms that control the production and
metabolism of superoxide anion (O(2)) and its interaction with
endothelium-derived nitric oxide (NO) that are of potential relevance to
signalling functions of (1) the normal coronary circulation and (2)
alterations in tissues derived from collaborations within the Program
Project on heart failure and exercise training. The second objective is
to determine how signalling mechanisms involved in the control coronary
vascular tone in normal arteries are altered by O(2))-NO interactions and
how changes in this interaction in vascular tissue derived from during
heart failure and exercise trained animals result in alterations in
mechanisms that control force generation. The third objective is to
elucidate the mechanism(s) involved in the control of cardiac (and
skeletal muscle) tissue respiration by endothelium-derived NO, with a
focus on the role of oxidant interactions in normal cardiac muscle and to
identify changes in the function of these processes in tissues derived
from the heart failure and exercise training models. Studies in this
project examining new signalling mechanisms will be conducted in isolated
calf coronary arteries, microvessels and cardiac muscle slices. The
collaborative studies focused on examining changes in signalling
mechanisms will be conducted on: isolated normal and failing dog coronary
arteries, microvessels and cardiac and skeletal muscle slices and isolated
normal and exercised rat aorta and skeletal muscle slices, and isolated
normal and failing human heart muscle. Collaborative studies on changes
in the activity, enzyme levels and mRNA of NO synthase and SOD enzymes
will also be employed to identify the origins of changes in the failure
and exercise training models. The results of these studies should provide
valuable information for understanding the role of oxidant and NO
interactions in the function of the coronary circulation, and in
identifying changes that occur in the role and mechanism of action of
these vascular function-related processes in heart failure and exercise
training.
这个项目的长期目标是发展对……的理解
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Michael S Wolin其他文献
Influence of heme metabolism and redox regulation of sGC in the control of vascular function
- DOI:
10.1186/1471-2210-7-s1-s33 - 发表时间:
2007-07-25 - 期刊:
- 影响因子:2.700
- 作者:
Michael S Wolin;Sachin A Gupte;Mansoor Ahmad;Christopher J Mingone - 通讯作者:
Christopher J Mingone
Michael S Wolin的其他文献
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{{ truncateString('Michael S Wolin', 18)}}的其他基金
ecSOD derived peroxide in pulmonary adaptation to hypoxia
ecSOD 衍生的过氧化物在肺适应缺氧中的作用
- 批准号:
8582142 - 财政年份:2013
- 资助金额:
$ 39.44万 - 项目类别:
ecSOD derived peroxide in pulmonary adaptation to hypoxia
ecSOD 衍生的过氧化物在肺适应缺氧中的作用
- 批准号:
9102162 - 财政年份:2013
- 资助金额:
$ 39.44万 - 项目类别:
ecSOD derived peroxide in pulmonary adaptation to hypoxia
ecSOD 衍生的过氧化物在肺适应缺氧中的作用
- 批准号:
8722598 - 财政年份:2013
- 资助金额:
$ 39.44万 - 项目类别:
Oxidants and Nitric Oxide in Coronary Vascular Function
氧化剂和一氧化氮对冠状血管功能的影响
- 批准号:
7252866 - 财政年份:2007
- 资助金额:
$ 39.44万 - 项目类别:
OXIDANTS AND NITRIC OXIDE IN CORONARY VASCULAR FUNCTION
冠状血管功能中的氧化剂和一氧化氮
- 批准号:
6931013 - 财政年份:2004
- 资助金额:
$ 39.44万 - 项目类别:
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