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Arginine vasopressin and pathophysiology of COVID-19: An innovative perspective - 09/10/21

Doi : 10.1016/j.biopha.2021.112193 
Hayder M. Al-kuraishy a , Ali I. Al-Gareeb a , Safaa Qusti b , Eida M. Alshammari c , Francis O. Atanu d , Gaber El-Saber Batiha e,
a Department of Clinical Pharmacology and Medicine, College of Medicine, ALmustansiriyia University, Baghdad, Iraq 
b Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia 
c Department of Chemistry, College of Sciences, University of Ha’il, Ha’il, Saudi Arabia 
d Department of Biochemistry, Faculty of Natural Sciences, Kogi State University, P.M.B. 1008 Anyigba, Nigeria 
e Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, AlBeheira, Egypt 

Corresponding author.

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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.

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Highlights

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.

El texto completo de este artículo está disponible en PDF.

Keywords : Covid-19, Arginine vasopressin, Hyponatremia


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© 2021  The Authors. Publicado por Elsevier Masson SAS. Todos los derechos reservados.
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Vol 143

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