ADENOSINE AND NITRIC OXIDE INTERACTION IN VASCULAR REGULATION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 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)确定在人体中抑制NO是否会导致静息状态下以及在氧气供应减少(缺血)或代谢需求增加(剧烈运动)时产生更多的ADO。 2)验证动脉粥样硬化高危和NO机制受损的患者基础ADO水平升高，ADO释放在缺血和运动中保持不变的假说。 3)在动脉粥样硬化高危和低危人群中，确定NO和Ado在局部血管调节中的作用。 4)在老年人和黑人中，确定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.