ADENOSINE AND NITRIC OXIDE INTERACTION IN VASCULAR REGULATION

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 当一氧化氮（NO）机制受损时，腺苷（Ado）是血管张力代谢调节的重要代偿机制。 具体目标 1)为了确定在人体中抑制NO是否会导致在休息时以及对氧气供应减少（缺血）或代谢需求增加（剧烈运动）的反应中Ado产生增加。 2)为了验证以下假设：在动脉粥样硬化和NO机制受损的高风险患者中，基础Ado水平增加，并且响应于缺血和运动而保持Ado释放。 3)确定动脉粥样硬化低风险和高风险受试者中NO和Ado对局部血管调节的贡献。 4)确定老年人和黑人中NO和Ado对局部血管调节的贡献。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Adenosine (Ado) is an important compensatory mechanism in the metabolic regulation of vascular tone when nitric oxide (NO) mechanisms are impaired. SPECIFIC AIMS 1) To determine if inhibition of NO in humans results in increased Ado production at rest and in response to decreased oxygen supply (ischemia) or increased metabolic demand (intense exercise). 2) To test the hypothesis that in patients w/high risk for atherosclerosis and impaired NO mechanisms, basal levels of Ado are increased, and Ado release is preserved in response to ischemia and exercise. 3) To determine, in subjects w/low and high risk for atherosclerosis, the contribution of NO and Ado to local vascular regulation. 4) To determine, in the elderly and in blacks, the contribution of NO and Ado to local vascular regulation.