ArticleAmerican journal of physiology. Cell physiology2011
Role of caveolin-1 in endothelial BKCa channel regulation of vasoreactivity.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- 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
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Single-cell transcriptomic heterogeneity between conduit and resistance mesenteric arteries in rats.Physiological genomics · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Endothelial cell membrane cholesterol content regulates the contribution of TRPV4 channels in ACh-induced vasodilation in rat gracilis arteries.Microcirculation (New York, N.Y. : 1994) · 2022Article
- Muscarinic Receptors and BK Channels Are Affected by Lipid Raft Disruption of Salivary Gland Cells.International journal of molecular sciences · 2021Article
- Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.Frontiers in physiology · 2021Review
- Coronary Large Conductance CaFrontiers in physiology · 2021Review
- The Membrane Cholesterol Modulates the Interaction Between 17-βEstradiol and the BK Channel.Frontiers in pharmacology · 2021Article
- Role of Transient Receptor Potential Vanilloid 4 in Vascular Function.Frontiers in molecular biosciences · 2021Review
- Long-term hypoxia uncouples CaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Endothelial-dependent dilation following chronic hypoxia involves TRPV4-mediated activation of endothelial BK channels.Pflugers Archiv : European journal of physiology · 2018Article
- Hydrogen sulfide-induced vasodilation mediated by endothelial TRPV4 channels.American journal of physiology. Heart and circulatory physiology · 2016Article
- Long-term hypoxia increases calcium affinity of BK channels in ovine fetal and adult cerebral artery smooth muscle.American journal of physiology. Heart and circulatory physiology · 2015Article
- Article
- Caveolin-1 limits the contribution of BKCa channel to MCF-7 breast cancer cell proliferation and invasion.International journal of molecular sciences · 2014Article
- Silencing of Kir2 channels by caveolin-1: cross-talk with cholesterol.The Journal of physiology · 2014Article
- Sarcolemmal cholesterol and caveolin-3 dependence of cardiac function, ischemic tolerance, and opioidergic cardioprotection.American journal of physiology. Heart and circulatory physiology · 2014Article
- Aging increases capacitance and spontaneous transient outward current amplitude of smooth muscle cells from murine superior epigastric arteries.American journal of physiology. Heart and circulatory physiology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A novel vasodilatory influence of endothelial cell (EC) large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels is present following 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. We tested the hypothesis that CH removes an inhibitory effect of the scaffolding domain of caveolin-1 (Cav-1) on EC BK(Ca) channels to permit activation, thereby affecting vasoreactivity. Experiments were performed on gracilis resistance arteries and ECs from control and CH-exposed (380 mmHg barometric pressure for 48 h) rats. EC membrane potential was hyperpolarized in arteries from CH-exposed rats and arteries treated with the cholesterol-depleting agent methyl-β-cyclodextrin (MBCD) compared with controls. Hyperpolarization was reversed by the BK(Ca) channel antagonist iberiotoxin (IBTX) or by a scaffolding domain peptide of Cav-1 (AP-CAV). Patch-clamp experiments documented an IBTX-sensitive current in ECs from CH-exposed rats and in MBCD-treated cells that was not present in controls. This current was enhanced by the BK(Ca) channel activator NS-1619 and blocked by AP-CAV or cholesterol supplementation. EC BK(Ca) channels displayed similar unitary conductance but greater Ca(2+) sensitivity than BK(Ca) channels from vascular smooth muscle. Immunofluorescence imaging demonstrated greater association of BK(Ca) α-subunits with Cav-1 in control arteries than in arteries from CH-exposed rats, although fluorescence intensity for each protein did not differ between groups. Finally, AP-CAV restored myogenic and phenylephrine-induced constriction in arteries from CH-exposed rats without affecting controls. AP-CAV similarly restored diminished reactivity to phenylephrine in control arteries pretreated with MBCD. We conclude that CH unmasks EC BK(Ca) channel activity by removing an inhibitory action of the Cav-1 scaffolding domain that may depend on cellular cholesterol levels.
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