ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Novel role of endothelial BKCa channels in altered vasoreactivity following hypoxia.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Effects of SGLT2 inhibitors on ion channels in heart failure: focus on the endothelium.Basic research in cardiology · 2025Review
- 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
- Vascular mechanotransduction.Physiological reviews · 2023Review
- CaInternational journal of molecular sciences · 2023Review
- Role of Cholesterol in the Regulation of Hydrogen Sulfide Signaling within the Vascular Endothelium.Antioxidants (Basel, Switzerland) · 2022Article
- 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
- Skin Microhemodynamics and Mechanisms of Its Regulation in Type 2 Diabetes Mellitus.Biophysics · 2022Article
- Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.Frontiers in physiology · 2021Review
- Coronary Large Conductance CaFrontiers in physiology · 2021Review
- Identification of molecular mechanism underlying therapeutic effect of tanshinone IIA in the treatment of hypoxic vestibular vertigo via the NO/cGMP/BKCa signaling pathway.American journal of translational research · 2019Article
- 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
- Calycosin and Formononetin Induce Endothelium-Dependent Vasodilation by the Activation of Large-Conductance CaEvidence-based complementary and alternative medicine : eCAM · 2016Article
- Endothelium-Derived Hyperpolarization and Coronary Vasodilation: Diverse and Integrated Roles of Epoxyeicosatrienoic Acids, Hydrogen Peroxide, and Gap Junctions.Microcirculation (New York, N.Y. : 1994) · 2016Review
- Decreased calcium-activated potassium channels by hypoxia causes abnormal firing in the spontaneous firing medial vestibular nuclei neurons.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2015Article
- Impairment of IKCa channels contributes to uteroplacental endothelial dysfunction in rat diabetic pregnancy.American journal of physiology. Heart and circulatory physiology · 2015Article
- 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
- 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
5 authors at 1 institution in 1 country.
Funding
Abstract
The systemic vasculature exhibits attenuated vasoconstriction following hypobaric chronic hypoxia (CH) that is associated with endothelium-dependent vascular smooth muscle (VSM) cell hyperpolarization. We hypothesized that increased activity of endothelial cell (EC) large-conductance, calcium-activated potassium (BK(Ca)) channels contributes to this response. Gracilis resistance arteries from hypobaric CH (barometric pressure = 380 mmHg for 48 h) rats demonstrated reduced myogenic reactivity and hyperpolarized VSM membrane potential (E(m)) compared with controls under normoxic ex vivo conditions. These differences were eliminated by endothelial disruption. In the presence of cyclooxygenase and nitric oxide synthase inhibition, combined intraluminal administration of the intermediate and small-conductance, calcium-activated K(+) channel blockers TRAM-34 and apamin was without effect on myogenic responsiveness and VSM E(m) in both groups; however, these variables were normalized in CH arteries by intraluminal administration of the BK(Ca) inhibitor iberiotoxin (IBTX). Basal EC E(m) was hyperpolarized in arteries from CH rats compared with controls and was restored by IBTX, but not by TRAM-34/apamin. K(+) channel blockers were without effect on EC basal E(m) in controls. Similarly, IBTX blocked acetylcholine-induced dilation in arteries from CH rats, but was without effect in controls, whereas TRAM-34/apamin eliminated dilation in controls. Acetylcholine-induced EC hyperpolarization and calcium responses were inhibited by IBTX in CH arteries and by TRAM-34/apamin in controls. Patch-clamp experiments on freshly isolated ECs demonstrated greater K(+) current in cells from CH rats that was normalized by IBTX. IBTX was without effect on K(+) current in controls. We conclude that hypobaric CH induces increased endothelial BK(Ca) channel activity that contributes to reduced myogenic responsiveness and EC and VSM cell hyperpolarization.
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