ArticleHypertension (Dallas, Tex. : 1979)2011
Distinct endothelium-derived hyperpolarizing factors emerge in vitro and in vivo and are mediated in part via connexin 40-dependent myoendothelial coupling.
Article in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 46 citations in OpenAlex.
- cGMP Signaling in Arterioles Revealed by FRET-Based Real-Time Measurement in Mice In Vivo.Acta physiologica (Oxford, England) · 2026Article
- The machinery of healthy vasodilatation: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- The conducted vasomotor response and the principles of electrical communication in resistance arteries.Physiological reviews · 2024Review
- Myography of isolated blood vessels: Considerations for experimental design and combination with supplementary techniques.Frontiers in physiology · 2023Review
- Mechanisms underlying selective coupling of endothelial CaThe Journal of physiology · 2020Article
- Endothelium-Derived Hyperpolarizing Factor and Myoendothelial Coupling: TheFrontiers in physiology · 2020Review
- Interactions between renal vascular resistance and endothelium-derived hyperpolarization in hypertensive rats in vivo.Physiological reports · 2019Article
- Endothelial connexins in vascular function.Vascular biology (Bristol, England) · 2019Review
- Connexins and Pannexins in Vascular Function and Disease.International journal of molecular sciences · 2018Review
- Intravital investigation of rat mesenteric small artery tone and blood flow.The Journal of physiology · 2017Article
- Contribution of K(+) channels to endothelium-derived hypolarization-induced renal vasodilation in rats in vivo and in vitro.Pflugers Archiv : European journal of physiology · 2016Article
- Clusters of specialized detector cells provide sensitive and high fidelity receptor signaling in the intact endothelium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Origins of variation in conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2015Article
- Perturbation of chemical coupling by an endothelial Cx40 mutant attenuates endothelium-dependent vasodilation by KCa channels and elevates blood pressure in mice.Pflugers Archiv : European journal of physiology · 2015Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- The myoendothelial junction: connections that deliver the message.Physiology (Bethesda, Md.) · 2014Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Activation of KCa3.1 by SKA-31 induces arteriolar dilatation and lowers blood pressure in normo- and hypertensive connexin40-deficient mice.British journal of pharmacology · 2013Article
- High flow conditions increase connexin43 expression in a rat arteriovenous and angioinductive loop model.PloS one · 2013Article
- Transient receptor potential canonical type 3 channels facilitate endothelium-derived hyperpolarization-mediated resistance artery vasodilator activity.Cardiovascular research · 2012Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The endothelium-derived hyperpolarizing factor (EDHF) contributes critically to the regulation of vascular tone. Its dependency on direct signaling through myoendothelial gap junctions composed of connexins (Cx) is controversially discussed. We studied the impact of Cx40 in EDHF-type dilations in vivo and in vitro (wire and pressure myography) in small arteries (A. gracilis) using different Cx40-deficient mouse models. Acetylcholine induced prominent EDHF-type dilations (inhibition of NO synthase and cyclooxygenase) of ≈90% (maximum effect) in wild-type and Cx40-deficient vessels (Cx40-/-) in vitro under isobaric conditions. In contrast, under isometric conditions, EDHF-type relaxations were nearly abrogated in Cx40-/- (9±3%) but only slightly reduced in wild-type vessels (45±4%; P<0.05). Vessels expressing Cx45 instead of Cx40 exhibited similarly reduced relaxations (13±1%), demonstrating that Cx45 cannot replace Cx40 functionally. The necessity of Cx40 in EDHF-type dilations under isometric conditions was verified by the attenuation in vessels being specifically deficient for Cx40 in endothelial cells (Cx40fl:TIE2-Cre: 17±3%; Cx40-floxed controls: 67±6%; P<0.05). Nevertheless, EDHF-type dilations were Cx40 independent when studied isobarically. The EDHF-type dilation in vivo resembled the isobaric situation, being virtually Cx40 independent and similar powerful. Distinct EDHF mechanisms can be distinguished by their Cx40 dependency. A powerful EDHF is present in vivo and in vitro under isobaric conditions but is lacking in wire myography (isometric conditions). Herein, a less potent EDHF depends on Cx40 and may represent signaling through myoendothelial gap junctions. We suggest that distinct EDHFs (even in the same artery) explain partially the controversy on the role of myoendothelial gap junctions in EDHF signaling.
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