Physiological role of endothelin-1 in flow-mediated vasodilatation in humans and impact of cardiovascular risk factors
The current study addressed the hypothesis that the local decrease in endothelin-1 (ET-1) bioavailability during sustained flow increases contributes to endothelium-dependent, flow-mediated dilatation (FMD) of conduit arteries and is altered in presence of cardiovascular risk factors. In nine young...
Gespeichert in:
| Veröffentlicht in: | Journal of hypertension 2017-06, Vol.35 (6), p.1204-1212 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1212 |
|---|---|
| container_issue | 6 |
| container_start_page | 1204 |
| container_title | Journal of hypertension |
| container_volume | 35 |
| creator | Bellien, Jérémy Iacob, Michèle Monteil, Christelle Rémy-Jouet, Isabelle Roche, Clothilde Duflot, Thomas Vendeville, Cathy Gutierrez, Laurence Thuillez, Christian Richard, Vincent Joannidès, Robinson |
| description | The current study addressed the hypothesis that the local decrease in endothelin-1 (ET-1) bioavailability during sustained flow increases contributes to endothelium-dependent, flow-mediated dilatation (FMD) of conduit arteries and is altered in presence of cardiovascular risk factors.
In nine young healthy individuals, the decrease in local ET-1 plasma levels and radial artery FMD in response to hand skin heating (from 34 to 44 °C) was not affected by endothelin type A (ETA) receptor blockade, achieved using the brachial infusion of BQ-123 (100 nmol/min per l of forearm), as compared with physiological saline (0.9% NaCl) infusion. In contrast, endothelin type B (ETB) receptor blockade with BQ-788 (10 nmol/min per l) suppressed the decrease in plasma ET-1 during heating and reduced FMD, without altering nitric oxide release. The coinfusion of BQ-123 did not affect the inhibitory effect of ETB receptor blockade on the decrease in ET-1 plasma levels during heating but prevented the reduction in FMD. Basal radial artery parameters, systemic hemodynamics, and endothelium-independent dilatation to glyceryl trinitrate were not modified by ETA and/or ETB blockade. In a general population of 40 participants without treatment or major cardiovascular diseases, including the nine healthy individuals, the reduction in endothelin-1 level during heating was correlated with FMD (r = -0.55, P |
| doi_str_mv | 10.1097/HJH.0000000000001307 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_02300714v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1892332247</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1862-8dc01d95767ee5be584cddc4d0cf9f8b13c3d1a5f7394b6d65c586ad87f783a53</originalsourceid><addsrcrecordid>eNpdkU1rGzEQhkVpaRy3_yAUHdvDpvpYrbTHEJI4xZAc0rMY66NWol250q6L_33X2DEhcxmY95l3YF6ELii5pKSVPxe_FpfkTVFO5Ac0o7XklRCt-ohmhDW8arhgZ-i8lOcJUq3kn9EZU3VNm5bN0PZxvSshxfQnGIg4p-hw8tj1Ng1rF0NfURx67GP6V3XOBhicxVsoyYYIAwwh9Xt9PXbQFwy9xaHbgBn2JgayDWmCzRgh4xzKC_aTlnL5gj55iMV9PfY5-n1783S9qJYPd_fXV8vKUNWwSllDqG2FbKRzYuWEqo21prbE-NarFeWGWwrCS97Wq8Y2wgjVgFXSS8VB8Dn6cfBdQ9SbHDrIO50g6MXVUu9nhHFCJK23dGK_H9hNTn9HVwbdhWJcjNC7NBZNVcs4Z2x68BzVB9TkVEp2_uRNid6no6d09Pt0prVvxwvjanrmaek1Dv4fytmLgw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1892332247</pqid></control><display><type>article</type><title>Physiological role of endothelin-1 in flow-mediated vasodilatation in humans and impact of cardiovascular risk factors</title><source>MEDLINE</source><source>Journals@Ovid Complete</source><creator>Bellien, Jérémy ; Iacob, Michèle ; Monteil, Christelle ; Rémy-Jouet, Isabelle ; Roche, Clothilde ; Duflot, Thomas ; Vendeville, Cathy ; Gutierrez, Laurence ; Thuillez, Christian ; Richard, Vincent ; Joannidès, Robinson</creator><creatorcontrib>Bellien, Jérémy ; Iacob, Michèle ; Monteil, Christelle ; Rémy-Jouet, Isabelle ; Roche, Clothilde ; Duflot, Thomas ; Vendeville, Cathy ; Gutierrez, Laurence ; Thuillez, Christian ; Richard, Vincent ; Joannidès, Robinson</creatorcontrib><description>The current study addressed the hypothesis that the local decrease in endothelin-1 (ET-1) bioavailability during sustained flow increases contributes to endothelium-dependent, flow-mediated dilatation (FMD) of conduit arteries and is altered in presence of cardiovascular risk factors.
In nine young healthy individuals, the decrease in local ET-1 plasma levels and radial artery FMD in response to hand skin heating (from 34 to 44 °C) was not affected by endothelin type A (ETA) receptor blockade, achieved using the brachial infusion of BQ-123 (100 nmol/min per l of forearm), as compared with physiological saline (0.9% NaCl) infusion. In contrast, endothelin type B (ETB) receptor blockade with BQ-788 (10 nmol/min per l) suppressed the decrease in plasma ET-1 during heating and reduced FMD, without altering nitric oxide release. The coinfusion of BQ-123 did not affect the inhibitory effect of ETB receptor blockade on the decrease in ET-1 plasma levels during heating but prevented the reduction in FMD. Basal radial artery parameters, systemic hemodynamics, and endothelium-independent dilatation to glyceryl trinitrate were not modified by ETA and/or ETB blockade. In a general population of 40 participants without treatment or major cardiovascular diseases, including the nine healthy individuals, the reduction in endothelin-1 level during heating was correlated with FMD (r = -0.55, P < 0.001) and decreased with increased age (r = 0.49, P = 0.001), mean arterial blood pressure (r = 0.48, P = 0.002), and total cholesterol level (r = 0.37, P = 0.024).
The uptake of endothelin-1 by ETB receptors contributes to conduit artery FMD, preventing its vasoconstrictor action mediated by ETA receptors. The alteration of this mechanism by cardiovascular risk factors may contribute to endothelial dysfunction.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/HJH.0000000000001307</identifier><identifier>PMID: 28441692</identifier><language>eng</language><publisher>England: Lippincott, Williams & Wilkins</publisher><subject>Adult ; Cardiology and cardiovascular system ; Cardiovascular Diseases ; Endothelin A Receptor Antagonists - pharmacology ; Endothelin B Receptor Antagonists - pharmacology ; Endothelin Receptor Antagonists - pharmacology ; Endothelin-1 - physiology ; Female ; Hemodynamics - physiology ; Human health and pathology ; Humans ; Life Sciences ; Male ; Nitric Oxide - metabolism ; Oligopeptides - pharmacology ; Peptides, Cyclic - pharmacology ; Piperidines - pharmacology ; Risk Factors ; Tissues and Organs ; Vasodilation - drug effects ; Vasodilation - physiology ; Young Adult</subject><ispartof>Journal of hypertension, 2017-06, Vol.35 (6), p.1204-1212</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1862-8dc01d95767ee5be584cddc4d0cf9f8b13c3d1a5f7394b6d65c586ad87f783a53</citedby><cites>FETCH-LOGICAL-c1862-8dc01d95767ee5be584cddc4d0cf9f8b13c3d1a5f7394b6d65c586ad87f783a53</cites><orcidid>0000-0002-8730-284X ; 0000-0002-4981-0800</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28441692$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://normandie-univ.hal.science/hal-02300714$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Bellien, Jérémy</creatorcontrib><creatorcontrib>Iacob, Michèle</creatorcontrib><creatorcontrib>Monteil, Christelle</creatorcontrib><creatorcontrib>Rémy-Jouet, Isabelle</creatorcontrib><creatorcontrib>Roche, Clothilde</creatorcontrib><creatorcontrib>Duflot, Thomas</creatorcontrib><creatorcontrib>Vendeville, Cathy</creatorcontrib><creatorcontrib>Gutierrez, Laurence</creatorcontrib><creatorcontrib>Thuillez, Christian</creatorcontrib><creatorcontrib>Richard, Vincent</creatorcontrib><creatorcontrib>Joannidès, Robinson</creatorcontrib><title>Physiological role of endothelin-1 in flow-mediated vasodilatation in humans and impact of cardiovascular risk factors</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>The current study addressed the hypothesis that the local decrease in endothelin-1 (ET-1) bioavailability during sustained flow increases contributes to endothelium-dependent, flow-mediated dilatation (FMD) of conduit arteries and is altered in presence of cardiovascular risk factors.
In nine young healthy individuals, the decrease in local ET-1 plasma levels and radial artery FMD in response to hand skin heating (from 34 to 44 °C) was not affected by endothelin type A (ETA) receptor blockade, achieved using the brachial infusion of BQ-123 (100 nmol/min per l of forearm), as compared with physiological saline (0.9% NaCl) infusion. In contrast, endothelin type B (ETB) receptor blockade with BQ-788 (10 nmol/min per l) suppressed the decrease in plasma ET-1 during heating and reduced FMD, without altering nitric oxide release. The coinfusion of BQ-123 did not affect the inhibitory effect of ETB receptor blockade on the decrease in ET-1 plasma levels during heating but prevented the reduction in FMD. Basal radial artery parameters, systemic hemodynamics, and endothelium-independent dilatation to glyceryl trinitrate were not modified by ETA and/or ETB blockade. In a general population of 40 participants without treatment or major cardiovascular diseases, including the nine healthy individuals, the reduction in endothelin-1 level during heating was correlated with FMD (r = -0.55, P < 0.001) and decreased with increased age (r = 0.49, P = 0.001), mean arterial blood pressure (r = 0.48, P = 0.002), and total cholesterol level (r = 0.37, P = 0.024).
The uptake of endothelin-1 by ETB receptors contributes to conduit artery FMD, preventing its vasoconstrictor action mediated by ETA receptors. The alteration of this mechanism by cardiovascular risk factors may contribute to endothelial dysfunction.</description><subject>Adult</subject><subject>Cardiology and cardiovascular system</subject><subject>Cardiovascular Diseases</subject><subject>Endothelin A Receptor Antagonists - pharmacology</subject><subject>Endothelin B Receptor Antagonists - pharmacology</subject><subject>Endothelin Receptor Antagonists - pharmacology</subject><subject>Endothelin-1 - physiology</subject><subject>Female</subject><subject>Hemodynamics - physiology</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Nitric Oxide - metabolism</subject><subject>Oligopeptides - pharmacology</subject><subject>Peptides, Cyclic - pharmacology</subject><subject>Piperidines - pharmacology</subject><subject>Risk Factors</subject><subject>Tissues and Organs</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Young Adult</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1rGzEQhkVpaRy3_yAUHdvDpvpYrbTHEJI4xZAc0rMY66NWol250q6L_33X2DEhcxmY95l3YF6ELii5pKSVPxe_FpfkTVFO5Ac0o7XklRCt-ohmhDW8arhgZ-i8lOcJUq3kn9EZU3VNm5bN0PZxvSshxfQnGIg4p-hw8tj1Ng1rF0NfURx67GP6V3XOBhicxVsoyYYIAwwh9Xt9PXbQFwy9xaHbgBn2JgayDWmCzRgh4xzKC_aTlnL5gj55iMV9PfY5-n1783S9qJYPd_fXV8vKUNWwSllDqG2FbKRzYuWEqo21prbE-NarFeWGWwrCS97Wq8Y2wgjVgFXSS8VB8Dn6cfBdQ9SbHDrIO50g6MXVUu9nhHFCJK23dGK_H9hNTn9HVwbdhWJcjNC7NBZNVcs4Z2x68BzVB9TkVEp2_uRNid6no6d09Pt0prVvxwvjanrmaek1Dv4fytmLgw</recordid><startdate>201706</startdate><enddate>201706</enddate><creator>Bellien, Jérémy</creator><creator>Iacob, Michèle</creator><creator>Monteil, Christelle</creator><creator>Rémy-Jouet, Isabelle</creator><creator>Roche, Clothilde</creator><creator>Duflot, Thomas</creator><creator>Vendeville, Cathy</creator><creator>Gutierrez, Laurence</creator><creator>Thuillez, Christian</creator><creator>Richard, Vincent</creator><creator>Joannidès, Robinson</creator><general>Lippincott, Williams & Wilkins</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-8730-284X</orcidid><orcidid>https://orcid.org/0000-0002-4981-0800</orcidid></search><sort><creationdate>201706</creationdate><title>Physiological role of endothelin-1 in flow-mediated vasodilatation in humans and impact of cardiovascular risk factors</title><author>Bellien, Jérémy ; Iacob, Michèle ; Monteil, Christelle ; Rémy-Jouet, Isabelle ; Roche, Clothilde ; Duflot, Thomas ; Vendeville, Cathy ; Gutierrez, Laurence ; Thuillez, Christian ; Richard, Vincent ; Joannidès, Robinson</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1862-8dc01d95767ee5be584cddc4d0cf9f8b13c3d1a5f7394b6d65c586ad87f783a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Cardiology and cardiovascular system</topic><topic>Cardiovascular Diseases</topic><topic>Endothelin A Receptor Antagonists - pharmacology</topic><topic>Endothelin B Receptor Antagonists - pharmacology</topic><topic>Endothelin Receptor Antagonists - pharmacology</topic><topic>Endothelin-1 - physiology</topic><topic>Female</topic><topic>Hemodynamics - physiology</topic><topic>Human health and pathology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Nitric Oxide - metabolism</topic><topic>Oligopeptides - pharmacology</topic><topic>Peptides, Cyclic - pharmacology</topic><topic>Piperidines - pharmacology</topic><topic>Risk Factors</topic><topic>Tissues and Organs</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bellien, Jérémy</creatorcontrib><creatorcontrib>Iacob, Michèle</creatorcontrib><creatorcontrib>Monteil, Christelle</creatorcontrib><creatorcontrib>Rémy-Jouet, Isabelle</creatorcontrib><creatorcontrib>Roche, Clothilde</creatorcontrib><creatorcontrib>Duflot, Thomas</creatorcontrib><creatorcontrib>Vendeville, Cathy</creatorcontrib><creatorcontrib>Gutierrez, Laurence</creatorcontrib><creatorcontrib>Thuillez, Christian</creatorcontrib><creatorcontrib>Richard, Vincent</creatorcontrib><creatorcontrib>Joannidès, Robinson</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bellien, Jérémy</au><au>Iacob, Michèle</au><au>Monteil, Christelle</au><au>Rémy-Jouet, Isabelle</au><au>Roche, Clothilde</au><au>Duflot, Thomas</au><au>Vendeville, Cathy</au><au>Gutierrez, Laurence</au><au>Thuillez, Christian</au><au>Richard, Vincent</au><au>Joannidès, Robinson</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Physiological role of endothelin-1 in flow-mediated vasodilatation in humans and impact of cardiovascular risk factors</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2017-06</date><risdate>2017</risdate><volume>35</volume><issue>6</issue><spage>1204</spage><epage>1212</epage><pages>1204-1212</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><abstract>The current study addressed the hypothesis that the local decrease in endothelin-1 (ET-1) bioavailability during sustained flow increases contributes to endothelium-dependent, flow-mediated dilatation (FMD) of conduit arteries and is altered in presence of cardiovascular risk factors.
In nine young healthy individuals, the decrease in local ET-1 plasma levels and radial artery FMD in response to hand skin heating (from 34 to 44 °C) was not affected by endothelin type A (ETA) receptor blockade, achieved using the brachial infusion of BQ-123 (100 nmol/min per l of forearm), as compared with physiological saline (0.9% NaCl) infusion. In contrast, endothelin type B (ETB) receptor blockade with BQ-788 (10 nmol/min per l) suppressed the decrease in plasma ET-1 during heating and reduced FMD, without altering nitric oxide release. The coinfusion of BQ-123 did not affect the inhibitory effect of ETB receptor blockade on the decrease in ET-1 plasma levels during heating but prevented the reduction in FMD. Basal radial artery parameters, systemic hemodynamics, and endothelium-independent dilatation to glyceryl trinitrate were not modified by ETA and/or ETB blockade. In a general population of 40 participants without treatment or major cardiovascular diseases, including the nine healthy individuals, the reduction in endothelin-1 level during heating was correlated with FMD (r = -0.55, P < 0.001) and decreased with increased age (r = 0.49, P = 0.001), mean arterial blood pressure (r = 0.48, P = 0.002), and total cholesterol level (r = 0.37, P = 0.024).
The uptake of endothelin-1 by ETB receptors contributes to conduit artery FMD, preventing its vasoconstrictor action mediated by ETA receptors. The alteration of this mechanism by cardiovascular risk factors may contribute to endothelial dysfunction.</abstract><cop>England</cop><pub>Lippincott, Williams & Wilkins</pub><pmid>28441692</pmid><doi>10.1097/HJH.0000000000001307</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8730-284X</orcidid><orcidid>https://orcid.org/0000-0002-4981-0800</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0263-6352 |
| ispartof | Journal of hypertension, 2017-06, Vol.35 (6), p.1204-1212 |
| issn | 0263-6352 1473-5598 |
| language | eng |
| recordid | cdi_hal_primary_oai_HAL_hal_02300714v1 |
| source | MEDLINE; Journals@Ovid Complete |
| subjects | Adult Cardiology and cardiovascular system Cardiovascular Diseases Endothelin A Receptor Antagonists - pharmacology Endothelin B Receptor Antagonists - pharmacology Endothelin Receptor Antagonists - pharmacology Endothelin-1 - physiology Female Hemodynamics - physiology Human health and pathology Humans Life Sciences Male Nitric Oxide - metabolism Oligopeptides - pharmacology Peptides, Cyclic - pharmacology Piperidines - pharmacology Risk Factors Tissues and Organs Vasodilation - drug effects Vasodilation - physiology Young Adult |
| title | Physiological role of endothelin-1 in flow-mediated vasodilatation in humans and impact of cardiovascular risk factors |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T23%3A31%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_hal_p&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Physiological%20role%20of%20endothelin-1%20in%20flow-mediated%20vasodilatation%20in%20humans%20and%20impact%20of%20cardiovascular%20risk%20factors&rft.jtitle=Journal%20of%20hypertension&rft.au=Bellien,%20J%C3%A9r%C3%A9my&rft.date=2017-06&rft.volume=35&rft.issue=6&rft.spage=1204&rft.epage=1212&rft.pages=1204-1212&rft.issn=0263-6352&rft.eissn=1473-5598&rft_id=info:doi/10.1097/HJH.0000000000001307&rft_dat=%3Cproquest_hal_p%3E1892332247%3C/proquest_hal_p%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1892332247&rft_id=info:pmid/28441692&rfr_iscdi=true |