Role of Nitric Oxide in the Regulation of Vascular Tone in Septic Shock

Septic shock is characterized by hypotension, decreased vascular reactivity to vasoconstrictor agents and an abnormal tissue oxygen extraction leading to a pathological supply-dependent oxygen consumption [1, 2]. Persistent vasodilation is a frequent cause of death among these patients, when their condition evolves and blood pressure can no longer be maintained by increasing doses of sympathomimetic agents [1]. The mechanisms involved in these abnormalities are incompletely understood. The discovery of the L-arginine nitric oxide pathway has greatly contributed to our current understanding of the pathophysiology of the hypotension and vascular hyporeactivity characteristics of septic shock.