Levosimendan exerts its vasodilatory effects in heart failure primarily through K+-channel opening and Ca2+ desensitization in vascular smooth muscle.
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Should not alter levosimendan use in HF; leaves open PDE inhibition contribution for targeted studies.
Levosimendan, a novel agent developed for the treatment of acute and decompensated heart failure, exerts potent positive inotropic action and peripheral vasodilatory effects. The mechanism of vasodilation by levosimendan may involve reduction of Ca2+ sensitivity of contractile proteins in vascular smooth muscle, the lowering of intracellular free Ca2+, the potential inhibition of phosphodiesterase (PDE) III, and an opening of K+ channels. Although the importance and relative contribution of each of these mechanisms of vasorelaxation is unclear and may be different in various vessels and dependent on the dose of levosimendan, the important roles of K+-channel opening and Ca2+ desensitization in vascular smooth muscle are obvious, whereas the role of PDE inhibition remains to be defined. This review article briefly discusses the current research data on the mechanism of levosimendan-induced vasodilation with an emphasis on the types of the blood vessels and the K+ channels. It also summarizes the current experimental and clinical knowledge of the use of levosimedan in the treatment of heart failure.
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Oğuzhan Yıldız (2007) studied this question.
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