In the search for treatments for critical illnesses, levosimendan has been found to be interesting candidate, as it is a potent stimulator of vascular ATP-dependent potassium channels (K ? -ATP channels), inducing systemic vasodilation and reducing afterload. Schwarte et al. [114] examined the effect of levosimendan on cardiac output and tissue perfusion in the presence of hypoxia in a canine model. They found that when levosimendan was infused before hypoxia was induced, myocardial contractility, stroke volume and cardiac output were preserved in spite of the hypoxic insult. The novelty of this study is the examination of the antagonising effect of glibenclamide on the action of levosimendan. When given alone, glibenclamide caused a rise in systemic vascular resistance, suggesting that glibenclamide was acting to block K ? -ATP channels. When levosimendan was administered in the presence of glibenclamide, levosimendan caused a significant rise in cardiac output by improving myocardial contractility. This is indicative of levosimendan acting through a calcium-sensitising effect rather than on K ? -ATP channels. In a separate study, Revermann et al. [115] reported that the administration of levosimendan and nicorandil (a K ? -channel opener) attenuated the increased pulmonary vascular medial wall thickness in a model of pulmonary hypertension induced by monocrotaline challenge. Levosimendan significantly diminished the proliferation of pulmonary arterial smooth muscle cells, and this effect was attenuated by glibenclamide. In cell culture, levosimendan had a direct inhibitory effect on the platelet-derived growth factor induced proliferation of pulmonary arterial smooth muscle cells. These findings of levosimendan exerting inotropic, vasodilatory and anti-inflammatory properties under experimental conditions are exciting, but the real promise for levosimendan as a therapeutic candidate to support critical illness remains to be elucidated. Further in vitro and animal studies are required to understand the vasodilatory action of levosimendan, and the consequent effects-positive or negative-on end-organ perfusion [116] . Acute kidney injury is a common complication in patients with sepsis.