Key result
Activation of endothelial SK(Ca) and IK(Ca) channels by NS309 and DCEBIO enhanced NO synthesis and left-shifted acetylcholine-mediated inhibition of myogenic tone (IC50 from 237 nM to 43-101 nM).
Why the study?
Do SKCa and IKCa channel openers enhance agonist-evoked endothelial nitric oxide synthesis and arteriolar vasodilation in preclinical models?
Population
Single human endothelial cells and isolated, pressurized arterioles from rat cremaster skeletal muscle
Comparison
SKCa and IKCa channel openers (NS309 and DCEBIO) vs Control (absence of openers)
Design
Preclinical
Authors
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May enhance resistance-vessel vasodilation via SKCa/IKCa; leaves open translation from animal models to human therapy.
Do SKCa and IKCa channel openers enhance agonist-evoked endothelial nitric oxide synthesis and arteriolar vasodilation in preclinical models?
Drug-induced enhancement of endothelial SKCa and IKCa channel activities represents a novel cellular mechanism to increase vasodilation of small-resistance arterioles, highlighting them as potential therapeutic targets.
Sheng et al. (2008) studied this question. NS309 and DCEBIO was evaluated on acetylcholine-mediated inhibition of myogenic tone. Activation of endothelial SK(Ca) and IK(Ca) channels by NS309 and DCEBIO enhanced NO synthesis and left-shifted acetylcholine-mediated inhibition of myogenic tone (IC50 from 237 nM to 43-101 nM).
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