RENIN-ANGIOTENSIN SYSTEM AND VASCULAR REACTIVITY IN SEVERE SEPSIS

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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. Sepsis is a systemic inflammatory response to infection, and is classified as severe sepsis when there is organ dysfunction. Microvascular reactivity to ischemia is impaired in severe sepsis, and is likely causal to altered perfusion and organ failure. The renin-angiotensin system is activated in sepsis, and there is mounting evidence that it contributes to the pathogenesis of sepsis in animal models. Because angiotensin II is a strong vasoconstrictor, it may contribute to impaired microvascular reactivity. This is a pilot study to evaluate the relationship between the renin-angiotensin system and microvascular function in human subjects with severe sepsis.