Several mechanisms have been proposed to explain vascular dysfunction induced by sepsis [110] . Experimental studies have shown that selective and nonselective inhibitors of vascular potassium (K ? ) channels increase arterial pressure or reverse shock-induced vascular hyporeactivity [111] . However, while the use of channel inhibitors remains an attractive option to counteract systemic vasodilation, it may also impair microcirculatory adaptation to shock [112] . Collin et al. [113] demonstrated that vascular K ? channels are activated and overexpressed, while their inhibition restores arterial pressure and vascular reactivity, and decreases lactate concentration, thus offering potential therapeutic perspectives for septic shock.