ArticleAmerican journal of physiology. Cell physiology2012
Regulation of endothelial BK channels by heme oxygenase-derived carbon monoxide and caveolin-1.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Hormone Replacement Therapy and Cardiovascular Health in Postmenopausal Women.International journal of molecular sciences · 2025Review
- Hypoxia and ischemic stroke modify cerebrovascular tone by upregulating endothelial BK(Ca) channels-Lessons from rat, pig, mouse, and human.Acta physiologica (Oxford, England) · 2025Article
- Single-cell transcriptomic heterogeneity between conduit and resistance mesenteric arteries in rats.Physiological genomics · 2023Article
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- [Carbon Monoxide and Pain Regulation: A Review].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021Review
- ET-CORM Mediated Vasorelaxation of Small Mesenteric Arteries: Involvement of Kv7 Potassium Channels.Frontiers in pharmacology · 2021Article
- Gas Signaling Molecules and Mitochondrial Potassium Channels.International journal of molecular sciences · 2018Review
- Endothelial-dependent dilation following chronic hypoxia involves TRPV4-mediated activation of endothelial BK channels.Pflugers Archiv : European journal of physiology · 2018Article
- Preconditioning with the BKAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels.American journal of physiology. Heart and circulatory physiology · 2016Article
- Signaling function of heme oxygenase proteins.Antioxidants & redox signaling · 2014Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Hydrogen sulfide dilates rat mesenteric arteries by activating endothelial large-conductance Ca²⁺-activated K⁺ channels and smooth muscle Ca²⁺ sparks.American journal of physiology. Heart and circulatory physiology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A novel vasodilatory influence of endothelial cell (EC) large-conductance Ca(2+)-activated K(+) (BK) channels is present after in vivo exposure to chronic hypoxia (CH) and may exist in other pathological states. However, the mechanism of channel activation that results in altered vasoreactivity is unknown. Previously, we demonstrated that inhibition of either BK channels or heme oxygenase (HO) restores vasoconstrictor reactivity after CH. Additionally, administration of the scaffolding domain of caveolin (Cav)-1 inhibits EC BK activity and restores vasoconstrictor reactivity in this setting. These results led us to hypothesize that CH exposure results in a loss in Cav-1 inhibition of EC BK channels, resulting in their activation by HO-derived carbon monoxide (CO). Experiments were conducted on freshly dispersed aortic ECs from control and CH-exposed (barometric pressure: 380 mmHg for 48 h) rats. In electrophysiology experiments, outward currents were greater in cells from CH rats as well as from cells from control rats treated with the cholesterol-depleting agent methyl-β-cyclodextrin. These enhanced currents were returned to control by HO inhibition. Channel activity could be restored by the CO donor CO-releasing molecule (CORM)-2 during HO inhibition. Administration of the Cav-1 scaffolding domain eliminated BK currents in cells from CH rats, and current was not restored by the addition of CORM-2. Colocalization experiments in ECs from control and CH rats demonstrated an association between HO-2, Cav-1, and BK. We conclude that EC BK channel activity is HO dependent in the absence of the inhibitory effect of the Cav-1 scaffolding domain.
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