title: Nitric oxide and vascular reactivity in sepsis.
abstract: Sepsis and septic shock are major causes of morbidity and mortality in critically ill patients. Sepsis and septic shock induce a profound fall in the peripheral vascular tone. NO has been implicated as a key player in vascular changes of sepsis and septic shock. In this brief review, two points are focused in greater detail: first, the involvement of guanylate cyclase and potassium channels in NO vascular effects in sepsis; second, the role played by NO and its two effectors in the long-lasting modifications of vascular reactivity in sepsis. Some recent developments in the area are reviewed.
authors.forename: Daniel
authors.initials: D
authors.lastname: Fernandes
authors.forename: Jamil
authors.initials: J
authors.lastname: Assreuy
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006162:Guanylate Cyclase / Q000378:metabolism*; D006801:Humans; D007249:Inflammation; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism*; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism*; D012772:Shock, Septic / Q000276:immunology / Q000378:metabolism; D013997:Time Factors
chemical_list: D015221:Potassium Channels; D009569:Nitric Oxide; D006162:Guanylate Cyclase