Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?
Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with...
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| Veröffentlicht in: | Molecular neurobiology 2019-10, Vol.56 (10), p.6792-6806 |
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| description | Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V
1
a
receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES. |
| doi_str_mv | 10.1007/s12035-019-1553-y |
| format | Article |
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1
a
receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-019-1553-y</identifier><identifier>PMID: 30924075</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Arginine Vasopressin - metabolism ; Argipressin ; Argipressin receptors ; Biomarkers - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Cell Biology ; Comorbidity ; Cytotoxicity ; Disease Susceptibility ; Eclampsia ; Edema ; Encephalopathy ; Human health and pathology ; Humans ; Ischemia ; Life Sciences ; Models, Biological ; Neurobiology ; Neurology ; Neurosciences ; Permeability ; Posterior Leukoencephalopathy Syndrome - pathology ; Posterior Leukoencephalopathy Syndrome - physiopathology ; Receptor density ; Secretion ; Sepsis ; Vasoconstriction ; Vasopressin</subject><ispartof>Molecular neurobiology, 2019-10, Vol.56 (10), p.6792-6806</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Molecular Neurobiology is a copyright of Springer, (2019). All Rights Reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c358t-4e526061ac9fbcb4ec0c9e6837ecb345b59d48e9fc81fd5bad07330c70514e63</cites><orcidid>0000-0001-5846-8616 ; 0000-0002-6824-7283 ; 0000-0001-8430-4543 ; 0000-0001-6221-4467 ; 0000-0001-9308-4933 ; 0000-0001-7675-9564</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-019-1553-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-019-1553-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,315,781,785,886,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30924075$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://nantes-universite.hal.science/hal-03183366$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Largeau, Bérenger</creatorcontrib><creatorcontrib>Le Tilly, Olivier</creatorcontrib><creatorcontrib>Sautenet, Bénédicte</creatorcontrib><creatorcontrib>Salmon Gandonnière, Charlotte</creatorcontrib><creatorcontrib>Barin-Le Guellec, Chantal</creatorcontrib><creatorcontrib>Ehrmann, Stephan</creatorcontrib><title>Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V
1
a
receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.</description><subject>Animals</subject><subject>Arginine Vasopressin - metabolism</subject><subject>Argipressin</subject><subject>Argipressin receptors</subject><subject>Biomarkers - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Cell Biology</subject><subject>Comorbidity</subject><subject>Cytotoxicity</subject><subject>Disease Susceptibility</subject><subject>Eclampsia</subject><subject>Edema</subject><subject>Encephalopathy</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Models, Biological</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Permeability</subject><subject>Posterior Leukoencephalopathy Syndrome - pathology</subject><subject>Posterior Leukoencephalopathy Syndrome - physiopathology</subject><subject>Receptor density</subject><subject>Secretion</subject><subject>Sepsis</subject><subject>Vasoconstriction</subject><subject>Vasopressin</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU1v1DAQhi0EokvhB3BBlrjAIeCP2Im5oFXVD6RFVFBxtRxnsnHJ2qmdrZR_j6OUIiFxssfzzOuZeRF6TckHSkj1MVFGuCgIVQUVghfzE7TJlxzRmj1FG1IrXlSyrE_Qi5RuCWGMkuo5OuFEsZJUYoP6bdw77zzgnyaFMUJKzmPjW3wd0gTRhYi_wz3E5JoB8Lm3MPZmCKOZ-hn_mH0bwwHwdQ7D2M_JhSHs50946gF_dYvYHu-c__X5JXrWmSHBq4fzFN1cnN-cXRW7b5dfzra7wnJRT0UJgkkiqbGqa2xTgiVWgax5BbbhpWiEassaVGdr2rWiMS2pOCe2IoKWIPkper_K5ib1GN3BxFkH4_TVdqeXN8JpzbmU9zSz71Z2jOHuCGnSB5csDIPxEI5JM5aXLJXgi-zbf9DbcIw-D6IZVWrZrBSZoitlY0gpQvfYASV6cUyvjunsmF4c03OuefOgfGwO0D5W_LEoA2wFUk75PcS_X_9f9TfsFaHG</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Largeau, Bérenger</creator><creator>Le Tilly, Olivier</creator><creator>Sautenet, Bénédicte</creator><creator>Salmon Gandonnière, Charlotte</creator><creator>Barin-Le Guellec, Chantal</creator><creator>Ehrmann, Stephan</creator><general>Springer US</general><general>Springer Nature B.V</general><general>Humana Press</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>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-5846-8616</orcidid><orcidid>https://orcid.org/0000-0002-6824-7283</orcidid><orcidid>https://orcid.org/0000-0001-8430-4543</orcidid><orcidid>https://orcid.org/0000-0001-6221-4467</orcidid><orcidid>https://orcid.org/0000-0001-9308-4933</orcidid><orcidid>https://orcid.org/0000-0001-7675-9564</orcidid></search><sort><creationdate>20191001</creationdate><title>Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?</title><author>Largeau, Bérenger ; Le Tilly, Olivier ; Sautenet, Bénédicte ; Salmon Gandonnière, Charlotte ; Barin-Le Guellec, Chantal ; Ehrmann, Stephan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c358t-4e526061ac9fbcb4ec0c9e6837ecb345b59d48e9fc81fd5bad07330c70514e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Arginine Vasopressin - metabolism</topic><topic>Argipressin</topic><topic>Argipressin receptors</topic><topic>Biomarkers - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Cell Biology</topic><topic>Comorbidity</topic><topic>Cytotoxicity</topic><topic>Disease Susceptibility</topic><topic>Eclampsia</topic><topic>Edema</topic><topic>Encephalopathy</topic><topic>Human health and pathology</topic><topic>Humans</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Models, Biological</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Permeability</topic><topic>Posterior Leukoencephalopathy Syndrome - pathology</topic><topic>Posterior Leukoencephalopathy Syndrome - physiopathology</topic><topic>Receptor density</topic><topic>Secretion</topic><topic>Sepsis</topic><topic>Vasoconstriction</topic><topic>Vasopressin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Largeau, Bérenger</creatorcontrib><creatorcontrib>Le Tilly, Olivier</creatorcontrib><creatorcontrib>Sautenet, Bénédicte</creatorcontrib><creatorcontrib>Salmon Gandonnière, Charlotte</creatorcontrib><creatorcontrib>Barin-Le Guellec, Chantal</creatorcontrib><creatorcontrib>Ehrmann, Stephan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Largeau, Bérenger</au><au>Le Tilly, Olivier</au><au>Sautenet, Bénédicte</au><au>Salmon Gandonnière, Charlotte</au><au>Barin-Le Guellec, Chantal</au><au>Ehrmann, Stephan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>56</volume><issue>10</issue><spage>6792</spage><epage>6806</epage><pages>6792-6806</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V
1
a
receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30924075</pmid><doi>10.1007/s12035-019-1553-y</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-5846-8616</orcidid><orcidid>https://orcid.org/0000-0002-6824-7283</orcidid><orcidid>https://orcid.org/0000-0001-8430-4543</orcidid><orcidid>https://orcid.org/0000-0001-6221-4467</orcidid><orcidid>https://orcid.org/0000-0001-9308-4933</orcidid><orcidid>https://orcid.org/0000-0001-7675-9564</orcidid></addata></record> |
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| subjects | Animals Arginine Vasopressin - metabolism Argipressin Argipressin receptors Biomarkers - metabolism Biomedical and Life Sciences Biomedicine Brain Cell Biology Comorbidity Cytotoxicity Disease Susceptibility Eclampsia Edema Encephalopathy Human health and pathology Humans Ischemia Life Sciences Models, Biological Neurobiology Neurology Neurosciences Permeability Posterior Leukoencephalopathy Syndrome - pathology Posterior Leukoencephalopathy Syndrome - physiopathology Receptor density Secretion Sepsis Vasoconstriction Vasopressin |
| title | Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link? |
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