Levosimendan Interacts with Potassium Channel Blockers in Human Saphenous Veins

Abstract

The involvement of potassium channels in the venodilating capacity of the inodilator levosimendan in human saphenous vein preparations was investigated. Levosimendan caused relaxation with 50% effective concentration (EC50) of 0.32 +/- 0.04 microM in isolated veins contracted by 5-hydroxytryptamine. Fifteen microM glibenclamide, a blocker of the ATP-sensitive potassium channels (K(ATP)), partially inhibited the relaxing effect of the inodilator. In the presence of iberiotoxin, the selective blocker of large conductance calcium-activated potassium channels (BK(Ca)), levosimendan induced contraction with EC50 of 0.21 +/- 0.06 microM. We presume that levosimendan dilates human saphenous veins by interacting with hyperpolarizing potassium channels (K(ATP) and BK(Ca)).

First experiences with intraoperative Levosimendan in pediatric cardiac surgery

“…Levosimendan is a calcium-sensitizing agent which has a relevant inotropic effect by sensitizing myocardial troponin C to calcium [3]. Additionally, Levosimendan is a vasodilator, stimulating adenosine triphosphate-dependent potassium channels of systemic, pulmonary, and coronary vascular smooth-muscle cells [2,6,7,10]. All of these properties are, theoretically, useful after pediatric cardiac surgery, but, so far, there are only very few clinical reports on its application in children [1,11].…”

Comparison of the Effects of Levosimendan and Papaverine on Human Internal Mammary Artery and Saphenous Vein

“…Its vasodilatory effect has been shown in some vascular beds including IMA [8] and SV [9]. Its vasodilatory action has been attributed to its opening effect on ATP-dependent potassium (K ATP ) channels of vascular smooth muscle cells [8,9].…”

Uso de levosimendana em diversos quadros de insuficiência cardíaca aguda

“…Beneficial effects of levosimendan are also related to its vasodilatory effects of systemic 18,19 , coronary [20][21][22] , pulmonary 23 , renal 19 , splanchnic 19 , and cerebral arteries 19 , and of systemic 18,24,25 and portal veins. 26 This effect is mediated by an adenosine tri-phosphate-(ATP) dependent potassium channel-opening effect in an ATP-dependent manner in arterial smooth muscle cells 27 of the small-resistance arteries and by a calcium-activated potassium and voltage-dependent potassium channel-opening effect in large conductance vessels 28,29 .…”