Key result
Nitric oxide induces pulmonary artery smooth muscle cell apoptosis, inhibited by K+ channel blockade.
Population
Human and rat pulmonary artery smooth muscle cells (PASMC)
Comparison
Nitric oxide derived from the NO donor… vs Control conditions
Design
Preclinical
Authors
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Hypothesis-generating for K+ channel modulation in pulmonary vascular apoptosis; leaves open in vivo translation and therapeutic relevance.
Nitric oxide induces apoptosis in pulmonary artery smooth muscle cells via activation of potassium channels and mitochondrial depolarization.
Krick et al. (2002) studied this question. Nitric oxide (NO) vs. K+ channel blockers (TEA, IBTX, 4-AP) or high extracellular K+ was evaluated on Apoptosis and K+ currents in pulmonary artery smooth muscle cells. Nitric oxide induces apoptosis in pulmonary artery smooth muscle cells, an effect significantly inhibited by blocking K+ channels with 1 mM TEA, 100 nM IBTX, or 5 mM 4-AP.
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