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  1. Article ; Online: Discovery of Nitric Oxide and Translation to Clinical Application.

    Félétou, Michel

    Physiology (Bethesda, Md.)

    2016  Volume 31, Issue 2, Page(s) 76–77

    MeSH term(s) Animals ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/metabolism ; Drug Design ; Endothelium/drug effects ; Endothelium/metabolism ; Humans ; Nitric Oxide/metabolism ; Signal Transduction/physiology
    Chemical Substances Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2016-03
    Publishing country United States
    Document type Editorial
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00056.2015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Endothelium-Dependent Hyperpolarization and Endothelial Dysfunction.

    Félétou, Michel

    Journal of cardiovascular pharmacology

    2016  Volume 67, Issue 5, Page(s) 373–387

    Abstract: The endothelium controls vascular tone not only by releasing various vasoactive substances but also by another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells and is termed endothelium-dependent ... ...

    Abstract The endothelium controls vascular tone not only by releasing various vasoactive substances but also by another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells and is termed endothelium-dependent hyperpolarization (EDH). These responses involve an increase in the endothelial intracellular Ca concentration by the activation of transient receptor potential channels (predominantly TRPV4) followed by the opening of Ca-activated K channels of small and intermediate conductance (SKCa and IKCa). These channels show a distinct subcellular distribution. SKCa are widely distributed over the plasma membrane but segregates at sites of homocellular endothelial junctions, whereas IKCa are preferentially expressed in the myoendothelial projections. Following KCa activation, smooth muscle hyperpolarization is evoked by electrical coupling through myoendothelial gap junctions and/or by the potassium efflux that subsequently activates smooth muscle Kir2.1 and/or Na/K-ATPase. Alteration of the EDH contributes to the endothelial dysfunctions observed in various pathologies or conversely compensates for the loss in NO bioavailability. A better characterization of EDH should allow determining whether new druggable targets can be identified for the treatment of cardiovascular diseases.
    MeSH term(s) Aging/physiology ; Animals ; Biological Factors/metabolism ; Calcium Channels/metabolism ; Cardiovascular Diseases/physiopathology ; Connexins/metabolism ; Diabetes Mellitus/physiopathology ; Endothelium, Vascular/metabolism ; Gap Junctions/metabolism ; Humans ; Membrane Potentials ; Muscle, Smooth, Vascular/metabolism ; Potassium Channels/metabolism ; Signal Transduction ; TRPV Cation Channels/metabolism
    Chemical Substances Biological Factors ; Calcium Channels ; Connexins ; Potassium Channels ; TRPV Cation Channels ; endothelium-dependent hyperpolarization factor
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0000000000000346
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book: EDHF

    Félétou, Michel / Vanhoutte, Paul M.

    the complete story

    2006  

    Author's details Michel Félétou ; Paul M. Vanhoutte
    Keywords Vasodilator Agents / pharmacology ; Biological Factors / pharmacology ; Endothelium, Vascular / drug effects ; Biological Factors / physiology ; Endothelium, Vascular / physiopathology ; Vascular endothelium ; Endothelins
    Subject code 612.13
    Language English
    Size 298 S. : Ill., graph. Darst.
    Publisher CRC Taylor & Francis
    Publishing place Boca Raton u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT014541371
    ISBN 978-0-415-33292-7 ; 0-415-33292-3
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2006 A 3243 order for loan Magazin

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  4. Article ; Online: Calcium-activated potassium channels and endothelial dysfunction: therapeutic options?

    Félétou, Michel

    British journal of pharmacology

    2009  Volume 156, Issue 4, Page(s) 545–562

    Abstract: The three subtypes of calcium-activated potassium channels (K(Ca)) of large, intermediate and small conductance (BK(Ca), IK(Ca) and SK(Ca)) are present in the vascular wall. In healthy arteries, BK(Ca) channels are preferentially expressed in vascular ... ...

    Abstract The three subtypes of calcium-activated potassium channels (K(Ca)) of large, intermediate and small conductance (BK(Ca), IK(Ca) and SK(Ca)) are present in the vascular wall. In healthy arteries, BK(Ca) channels are preferentially expressed in vascular smooth muscle cells, while IK(Ca) and SK(Ca) are preferentially located in endothelial cells. The activation of endothelial IK(Ca) and SK(Ca) contributes to nitric oxide (NO) generation and is required to elicit endothelium-dependent hyperpolarizations. In the latter responses, the hyperpolarization of the smooth muscle cells is evoked either via electrical coupling through myo-endothelial gap junctions or by potassium ions, which by accumulating in the intercellular space activate the inwardly rectifying potassium channel Kir2.1 and/or the Na(+)/K(+)-ATPase. Additionally, endothelium-derived factors such as cytochrome P450-derived epoxyeicosatrienoic acids and under some circumstances NO, prostacyclin, lipoxygenase products and hydrogen peroxide (H(2)O(2)) hyperpolarize and relax the underlying smooth muscle cells by activating BK(Ca). In contrast, cytochrome P450-derived 20-hydroxyeicosatetraenoic acid and various endothelium-derived contracting factors inhibit BK(Ca). Aging and cardiovascular diseases are associated with endothelial dysfunctions that can involve a decrease in NO bioavailability, alterations of EDHF-mediated responses and/or enhanced production of endothelium-derived contracting factors. Because potassium channels are involved in these endothelium-dependent responses, activation of endothelial and/or smooth muscle K(Ca) could prevent the occurrence of endothelial dysfunction. Therefore, direct activators of these potassium channels or compounds that regulate their activity or their expression may be of some therapeutic interest. Conversely, blockers of IK(Ca) may prevent restenosis and that of BK(Ca) channels sepsis-dependent hypotension.
    MeSH term(s) Animals ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Humans ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Nitric Oxide/metabolism ; Potassium Channels, Calcium-Activated/genetics ; Potassium Channels, Calcium-Activated/metabolism ; Potassium Channels, Calcium-Activated/physiology ; Vascular Diseases/drug therapy ; Vascular Diseases/metabolism ; Vascular Diseases/physiopathology ; Vasodilation/drug effects
    Chemical Substances Potassium Channels, Calcium-Activated ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2009-01-29
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/j.1476-5381.2009.00052.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book: The endothelium

    Félétou, Michel

    (Integrated systems physiology, from molecule to function to disease, ; #19-20)

    2011  

    Author's details Michel Félétou
    Series title Integrated systems physiology, from molecule to function to disease, ; #19-20
    MeSH term(s) Endothelium, Vascular/metabolism ; Endothelins ; Endothelial Cells ; Endothelium-Dependent Relaxing Factors ; Biological Factors/physiology
    Language English
    Size 2 v. :, ill. ;, 24 cm.
    Publisher Morgan & Claypool Life Sciences
    Publishing place San Rafael, Calif.
    Document type Book
    ISBN 9781615041237 ; 1615041230 ; 9781615043378 ; 1615043373
    Database Catalogue of the US National Library of Medicine (NLM)

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  6. Article: La collectrine : un nouveau composant du système rénine-angiotensine ?

    Bril, Antoine / Félétou, Michel

    Medecine sciences : M/S

    2014  Volume 30, Issue 2, Page(s) 136–139

    Title translation Collectrin: a new component of the renin-angiotensin system?.
    MeSH term(s) Animals ; Arginine/metabolism ; Essential Hypertension ; Humans ; Hypertension ; Kidney/metabolism ; Membrane Glycoproteins/physiology ; Mice ; Nitric Oxide/physiology ; Nitric Oxide Synthase/metabolism ; Renin-Angiotensin System/physiology ; Sodium/metabolism
    Chemical Substances CLTRN protein, human ; Membrane Glycoproteins ; Nitric Oxide (31C4KY9ESH) ; Arginine (94ZLA3W45F) ; Sodium (9NEZ333N27) ; Nitric Oxide Synthase (EC 1.14.13.39)
    Language French
    Publishing date 2014-02-24
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20143002007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Endothelium-dependent hyperpolarization: no longer an f-word!

    Félétou, Michel / Vanhoutte, Paul M

    Journal of cardiovascular pharmacology

    2013  Volume 61, Issue 2, Page(s) 91–92

    MeSH term(s) Biological Factors/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Terminology as Topic
    Chemical Substances Biological Factors ; endothelium-dependent hyperpolarization factor
    Language English
    Publishing date 2013-02
    Publishing country United States
    Document type Editorial
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0b013e31828197bc
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: EDHF: an update.

    Félétou, Michel / Vanhoutte, Paul M

    Clinical science (London, England : 1979)

    2009  Volume 117, Issue 4, Page(s) 139–155

    Abstract: The endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term 'endothelium-derived ... ...

    Abstract The endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term 'endothelium-derived hyperpolarizing factor' (EDHF). However, this acronym includes different mechanisms. Arachidonic acid metabolites derived from the cyclo-oxygenases, lipoxygenases and cytochrome P450 pathways, H(2)O(2), CO, H(2)S and various peptides can be released by endothelial cells. These factors activate different families of K(+) channels and hyperpolarization of the vascular smooth muscle cells contribute to the mechanisms leading to their relaxation. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca(2+) concentration of the endothelial cells, followed by the opening of SK(Ca) and IK(Ca) channels (small and intermediate conductance Ca(2+)-activated K(+) channels respectively). These channels have a distinct subcellular distribution: SK(Ca) are widely distributed over the plasma membrane, whereas IK(Ca) are preferentially expressed in the endothelial projections toward the smooth muscle cells. Following SK(Ca) activation, smooth muscle hyperpolarization is preferentially evoked by electrical coupling through myoendothelial gap junctions, whereas, following IK(Ca) activation, K(+) efflux can activate smooth muscle Kir2.1 and/or Na(+)/K(+)-ATPase. EDHF-mediated responses are altered by aging and various pathologies. Therapeutic interventions can restore these responses, suggesting that the improvement in the EDHF pathway contributes to their beneficial effect. A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases.
    MeSH term(s) Arachidonic Acid/metabolism ; Biological Factors/physiology ; Cardiovascular Diseases/physiopathology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiology ; Endothelium, Vascular/physiopathology ; Humans ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/physiology
    Chemical Substances Biological Factors ; endothelium-dependent hyperpolarization factor ; Arachidonic Acid (27YG812J1I)
    Language English
    Publishing date 2009-07-16
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20090096
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Hydrogen sulfide as an endothelium-derived hyperpolarizing factor in rodent mesenteric arteries.

    Edwards, Gillian / Félétou, Michel / Weston, Arthur H

    Circulation research

    2012  Volume 110, Issue 1, Page(s) e13–4; author reply e15–6

    MeSH term(s) Animals ; Endothelium, Vascular/metabolism ; Female ; Hydrogen Sulfide/metabolism ; KATP Channels/metabolism ; Male ; Vasodilation/physiology
    Chemical Substances KATP Channels ; Hydrogen Sulfide (YY9FVM7NSN)
    Language English
    Publishing date 2012-01-06
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.111.259309
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  10. Article ; Online: Nitric oxide: orchestrator of endothelium-dependent responses.

    Félétou, Michel / Köhler, Ralf / Vanhoutte, Paul M

    Annals of medicine

    2012  Volume 44, Issue 7, Page(s) 694–716

    Abstract: The present review first summarizes the complex chain of events, in endothelial and vascular smooth muscle cells, that leads to endothelium-dependent relaxations (vasodilatations) due to the generation of nitric oxide (NO) by endothelial nitric oxide ... ...

    Abstract The present review first summarizes the complex chain of events, in endothelial and vascular smooth muscle cells, that leads to endothelium-dependent relaxations (vasodilatations) due to the generation of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) and how therapeutic interventions may improve the bioavailability of NO and thus prevent/cure endothelial dysfunction. Then, the role of other endothelium-derived mediators (endothelium-derived hyperpolarizing (EDHF) and contracting (EDCF) factors, endothelin-1) and signals (myoendothelial coupling) is summarized also, with special emphasis on their interaction(s) with the NO pathway, which make the latter not only a major mediator but also a key regulator of endothelium-dependent responses.
    MeSH term(s) Biological Factors/metabolism ; Endothelin-1/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Muscle, Smooth, Vascular/metabolism ; Nitric Oxide/metabolism ; Signal Transduction/physiology ; Vasodilation/physiology
    Chemical Substances Biological Factors ; Endothelin-1 ; endothelium-dependent hyperpolarization factor ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2012-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1004226-x
    ISSN 1365-2060 ; 1651-2219 ; 0785-3890 ; 1743-1387
    ISSN (online) 1365-2060 ; 1651-2219
    ISSN 0785-3890 ; 1743-1387
    DOI 10.3109/07853890.2011.585658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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