Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective
In Covid-19, systemic disturbances may progress due to development of cytokine storm and dysregulation of and plasma osmolarility due to high release of pro-inflammatory cytokines and neuro-hormonal disorders. Arginine vasopressin (AVP) which is involve in the regulation of body osmotic system, body...
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Veröffentlicht in: | Biomedicine & pharmacotherapy 2021-11, Vol.143, p.112193-112193, Article 112193 |
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description | In Covid-19, systemic disturbances may progress due to development of cytokine storm and dysregulation of and plasma osmolarility due to high release of pro-inflammatory cytokines and neuro-hormonal disorders. Arginine vasopressin (AVP) which is involve in the regulation of body osmotic system, body water content, blood pressure and plasma volume, that are highly disturbed in Covid-19 and linked with poor clinical outcomes. Therefore, this present study aimed to find the potential association between AVP serum level and inflammatory disorders in Covid-19. It has been observed by different recent studies that physiological response due to fever, pain, hypovolemia, dehydration, and psychological stress is characterized by activation release of AVP to counter-balance high blood viscosity in Covid-19 patients. In addition, activated immune cells mainly T and B lymphocytes and released pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells, which in a vicious cycle trigger release of pro-inflammatory cytokines. Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit AVP-induced hyponatremia and release of pro-inflammatory cytokines in Covid-19. In conclusion, release of AVP from hypothalamus is augmented in Covid-19 due to stress, high pro-inflammatory cytokines, high circulating AngII and inhibition of GABAergic neurons. In turn, high AVP level leads to induction of hyponatremia, inflammatory disorders, and development of complications in Covid-19 by activation of NF-κB and NLRP3 inflammasome with release of pro-inflammatory cytokines. Therefore, AVP antagonists might be novel potential therapeutic modality in treating Covid-19 through mitigation of AVP-mediated inflammatory disorders and hyponatremia.
[Display omitted]
•Covid-19 is associated with dysregulation of plasma osmolarility due to release of cytokines and neuro-hormonal disorders.•Arginine vasopressin (AVP) is increased due to fever and dehydration to counter high blood viscosity in Covid-19 patients.•T and B lymphocytes as well as pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells in Covid-19.•High AVP levels lead to hyponatremia and inflammatory disorders by activation of NF-κB and NLRP3 inflammasome.•Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit progression of Covid-19. |
doi_str_mv | 10.1016/j.biopha.2021.112193 |
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[Display omitted]
•Covid-19 is associated with dysregulation of plasma osmolarility due to release of cytokines and neuro-hormonal disorders.•Arginine vasopressin (AVP) is increased due to fever and dehydration to counter high blood viscosity in Covid-19 patients.•T and B lymphocytes as well as pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells in Covid-19.•High AVP levels lead to hyponatremia and inflammatory disorders by activation of NF-κB and NLRP3 inflammasome.•Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit progression of Covid-19.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2021.112193</identifier><identifier>PMID: 34543987</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Arginine vasopressin ; Arginine Vasopressin - antagonists & inhibitors ; Arginine Vasopressin - metabolism ; Covid-19 ; COVID-19 - immunology ; COVID-19 - metabolism ; COVID-19 Drug Treatment ; Drug Discovery ; Humans ; Hyponatremia ; Inflammation - drug therapy ; Inflammation - metabolism ; SARS-CoV-2 ; Water-Electrolyte Imbalance - drug therapy</subject><ispartof>Biomedicine & pharmacotherapy, 2021-11, Vol.143, p.112193-112193, Article 112193</ispartof><rights>2021 The Authors</rights><rights>Copyright © 2021 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</rights><rights>2021 The Authors 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-e1baa0785e941568ddcf1da5c3f4efdeba3226a3e4555fcda8779de96bf08a533</citedby><cites>FETCH-LOGICAL-c463t-e1baa0785e941568ddcf1da5c3f4efdeba3226a3e4555fcda8779de96bf08a533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.biopha.2021.112193$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34543987$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Al-kuraishy, Hayder M.</creatorcontrib><creatorcontrib>Al-Gareeb, Ali I.</creatorcontrib><creatorcontrib>Qusti, Safaa</creatorcontrib><creatorcontrib>Alshammari, Eida M.</creatorcontrib><creatorcontrib>Atanu, Francis O.</creatorcontrib><creatorcontrib>Batiha, Gaber El-Saber</creatorcontrib><title>Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>In Covid-19, systemic disturbances may progress due to development of cytokine storm and dysregulation of and plasma osmolarility due to high release of pro-inflammatory cytokines and neuro-hormonal disorders. Arginine vasopressin (AVP) which is involve in the regulation of body osmotic system, body water content, blood pressure and plasma volume, that are highly disturbed in Covid-19 and linked with poor clinical outcomes. Therefore, this present study aimed to find the potential association between AVP serum level and inflammatory disorders in Covid-19. It has been observed by different recent studies that physiological response due to fever, pain, hypovolemia, dehydration, and psychological stress is characterized by activation release of AVP to counter-balance high blood viscosity in Covid-19 patients. In addition, activated immune cells mainly T and B lymphocytes and released pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells, which in a vicious cycle trigger release of pro-inflammatory cytokines. Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit AVP-induced hyponatremia and release of pro-inflammatory cytokines in Covid-19. In conclusion, release of AVP from hypothalamus is augmented in Covid-19 due to stress, high pro-inflammatory cytokines, high circulating AngII and inhibition of GABAergic neurons. In turn, high AVP level leads to induction of hyponatremia, inflammatory disorders, and development of complications in Covid-19 by activation of NF-κB and NLRP3 inflammasome with release of pro-inflammatory cytokines. Therefore, AVP antagonists might be novel potential therapeutic modality in treating Covid-19 through mitigation of AVP-mediated inflammatory disorders and hyponatremia.
[Display omitted]
•Covid-19 is associated with dysregulation of plasma osmolarility due to release of cytokines and neuro-hormonal disorders.•Arginine vasopressin (AVP) is increased due to fever and dehydration to counter high blood viscosity in Covid-19 patients.•T and B lymphocytes as well as pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells in Covid-19.•High AVP levels lead to hyponatremia and inflammatory disorders by activation of NF-κB and NLRP3 inflammasome.•Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit progression of Covid-19.</description><subject>Arginine vasopressin</subject><subject>Arginine Vasopressin - antagonists & inhibitors</subject><subject>Arginine Vasopressin - metabolism</subject><subject>Covid-19</subject><subject>COVID-19 - immunology</subject><subject>COVID-19 - metabolism</subject><subject>COVID-19 Drug Treatment</subject><subject>Drug Discovery</subject><subject>Humans</subject><subject>Hyponatremia</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>SARS-CoV-2</subject><subject>Water-Electrolyte Imbalance - drug therapy</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9Uctu2zAQJIoWjeP2D4pCx16kkCKpRw4FDOcJBPClyZVYkSubhkyqpCzAfx8ZdtP00tMusDszuzOEfGM0Y5QVV9ussb7fQJbTnGWM5azmH8iM1ZKmBaXlRzKjpeQp53l-QS5j3FJKZcGrz-SCCyl4XZUzslqEtXXWYTJC9H3AGK1LwJmkh2Ez8R-i9Z1fHxLfJsvVy-NNyurrZOES65wfYbAjJj2G2KM-9l_Ipxa6iF_PdU6e725_LR_Sp9X943LxlGpR8CFF1gDQspJYCyaLyhjdMgNS81Zga7CB6eoCOAopZasNVGVZG6yLpqUVSM7n5OeJt983OzQa3RCgU32wOwgH5cGqfyfObtTaj6oSguZcTgQ_zgTB_95jHNTORo1dBw79PqpclpIWknExrYrTqg4-xoDtmwyj6piF2qpTFuqYhTplMcG-vz_xDfTH_L8_4GTUaDGoqC06jcaGyU1lvP2_wiup6J6C</recordid><startdate>20211101</startdate><enddate>20211101</enddate><creator>Al-kuraishy, Hayder M.</creator><creator>Al-Gareeb, Ali I.</creator><creator>Qusti, Safaa</creator><creator>Alshammari, Eida M.</creator><creator>Atanu, Francis O.</creator><creator>Batiha, Gaber El-Saber</creator><general>Elsevier Masson SAS</general><general>The Author(s). Published by Elsevier Masson SAS</general><scope>6I.</scope><scope>AAFTH</scope><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>5PM</scope></search><sort><creationdate>20211101</creationdate><title>Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective</title><author>Al-kuraishy, Hayder M. ; Al-Gareeb, Ali I. ; Qusti, Safaa ; Alshammari, Eida M. ; Atanu, Francis O. ; Batiha, Gaber El-Saber</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-e1baa0785e941568ddcf1da5c3f4efdeba3226a3e4555fcda8779de96bf08a533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Arginine vasopressin</topic><topic>Arginine Vasopressin - antagonists & inhibitors</topic><topic>Arginine Vasopressin - metabolism</topic><topic>Covid-19</topic><topic>COVID-19 - immunology</topic><topic>COVID-19 - metabolism</topic><topic>COVID-19 Drug Treatment</topic><topic>Drug Discovery</topic><topic>Humans</topic><topic>Hyponatremia</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>SARS-CoV-2</topic><topic>Water-Electrolyte Imbalance - drug therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Al-kuraishy, Hayder M.</creatorcontrib><creatorcontrib>Al-Gareeb, Ali I.</creatorcontrib><creatorcontrib>Qusti, Safaa</creatorcontrib><creatorcontrib>Alshammari, Eida M.</creatorcontrib><creatorcontrib>Atanu, Francis O.</creatorcontrib><creatorcontrib>Batiha, Gaber El-Saber</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>PubMed Central (Full Participant titles)</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Al-kuraishy, Hayder M.</au><au>Al-Gareeb, Ali I.</au><au>Qusti, Safaa</au><au>Alshammari, Eida M.</au><au>Atanu, Francis O.</au><au>Batiha, Gaber El-Saber</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2021-11-01</date><risdate>2021</risdate><volume>143</volume><spage>112193</spage><epage>112193</epage><pages>112193-112193</pages><artnum>112193</artnum><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>In Covid-19, systemic disturbances may progress due to development of cytokine storm and dysregulation of and plasma osmolarility due to high release of pro-inflammatory cytokines and neuro-hormonal disorders. Arginine vasopressin (AVP) which is involve in the regulation of body osmotic system, body water content, blood pressure and plasma volume, that are highly disturbed in Covid-19 and linked with poor clinical outcomes. Therefore, this present study aimed to find the potential association between AVP serum level and inflammatory disorders in Covid-19. It has been observed by different recent studies that physiological response due to fever, pain, hypovolemia, dehydration, and psychological stress is characterized by activation release of AVP to counter-balance high blood viscosity in Covid-19 patients. In addition, activated immune cells mainly T and B lymphocytes and released pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells, which in a vicious cycle trigger release of pro-inflammatory cytokines. Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit AVP-induced hyponatremia and release of pro-inflammatory cytokines in Covid-19. In conclusion, release of AVP from hypothalamus is augmented in Covid-19 due to stress, high pro-inflammatory cytokines, high circulating AngII and inhibition of GABAergic neurons. In turn, high AVP level leads to induction of hyponatremia, inflammatory disorders, and development of complications in Covid-19 by activation of NF-κB and NLRP3 inflammasome with release of pro-inflammatory cytokines. Therefore, AVP antagonists might be novel potential therapeutic modality in treating Covid-19 through mitigation of AVP-mediated inflammatory disorders and hyponatremia.
[Display omitted]
•Covid-19 is associated with dysregulation of plasma osmolarility due to release of cytokines and neuro-hormonal disorders.•Arginine vasopressin (AVP) is increased due to fever and dehydration to counter high blood viscosity in Covid-19 patients.•T and B lymphocytes as well as pro-inflammatory cytokines stimulate discharge of stored AVP from immune cells in Covid-19.•High AVP levels lead to hyponatremia and inflammatory disorders by activation of NF-κB and NLRP3 inflammasome.•Vasopressin receptor antagonists have antiviral and anti-inflammatory effects that may inhibit progression of Covid-19.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>34543987</pmid><doi>10.1016/j.biopha.2021.112193</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Arginine vasopressin Arginine Vasopressin - antagonists & inhibitors Arginine Vasopressin - metabolism Covid-19 COVID-19 - immunology COVID-19 - metabolism COVID-19 Drug Treatment Drug Discovery Humans Hyponatremia Inflammation - drug therapy Inflammation - metabolism SARS-CoV-2 Water-Electrolyte Imbalance - drug therapy |
title | Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective |
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