The levosimendan metabolite OR‐1896 elicits vasodilation by activating the KATPand BKCachannels in rat isolated arterioles
Key result
OR-1896 elicited concentration-dependent dilations in rat coronary and gracilis muscle arterioles (maximal dilations 66% and 73%, respectively), comparable to levosimendan.
Population
Isolated, pressurized (80 mmHg) rat coronary and gracilis muscle arterioles (approximately 150 microm)
Comparison
OR-1896 (1 nM-10 microM) vs Levosimendan and various K+ channel inhibitors
Design
Preclinical
Authors
Discussion
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Implication
May contribute to levosimendan effects in rats; hypothesis-generating before human translation.
Structured PICO
P
Population
Isolated, pressurized (80 mmHg) rat coronary and gracilis muscle arterioles (approximately 150 microm)
I
Intervention
OR-1896 (1 nM-10 microM)
C
Comparator
Levosimendan (1 nM-10 microM) and various K+ channel inhibitors (tetraethylammonium, glibenclamide, iberiotoxin)
O
Outcome
Arteriole diameter (vasodilation)surrogate
Main Result
Absolute Event Rate: 66% vs 83%
OR-1896, the long-lived metabolite of levosimendan, elicits substantial vasodilation in coronary and skeletal muscle arterioles via activation of BK(Ca) and K(ATP) channels, likely contributing to the drug's long-term hemodynamic effects.
Cite This Study
Erdei et al. (2006) studied this question. OR-1896 vs. Levosimendan was evaluated on Maximal dilation in coronary arterioles. OR-1896 elicited concentration-dependent dilations in rat coronary and gracilis muscle arterioles (maximal dilations 66% and 73%, respectively), comparable to levosimendan.