NOS2 and Sepsis: While these mechanisms dominate at the microvascular level in early or localized sepsis, progression to septic shock is characterized by robust inducible NOS (iNOS) induction, leading to massive •NO release, systemic vasorelaxation, hypotension, and diminished responsiveness to vasoactive stimuli, bridging the gap between experimental observations and the clinical hemodynamic collapse observed in patients [35,157].