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This paper attempts to explain how the SARS-CoV-2 virus causes the complications that make COVID-19 a serious disease in specific patient subgroups. It suggests that cortisol-associated activation of the Mineralocorticoid Receptor (MR) in epithelial and endothelial cells infected with the virus stimulates the release of ATP which then acts back on purinergic receptors. In the lung this could produce the non-productive cough via purinergic P2X3 receptors on vagal afferent nerves. In endothelial cells it could stimulate exocytosis of Weibel-Palade (WP) bodies that contain angiopoietin-2 which is important in the pathogenesis of the Acute Respiratory Distress Syndrome (ARDS) by increasing capillary permeability and Von Willebrand Factor which mediates platelet adhesion to the endothelium and hence clotting. Both angiopoietin-2 and VWF levels are markedly elevated in COVID-19 associated ARDS. The paper offers an explanation for the sex differences in SARS-CoV-2 complications and also for why these are strongly associated with age, race, diabetes and body mass index. It also explains why individuals with blood group A have a higher risk of severe infection than those with blood group O. Dexamethasone has been shown to be of benefit in coronavirus ARDS patients and has been thought to act as an anti-inflammatory drug. This paper suggests that a major part of its effect may be due to suppression of cortisol secretion. There is an urgent need to trial the combination of dexamethasone and an MR antagonist such as spironolactone to more effectively block the MR and hence the exocytosis of WP bodies.
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New Horizons: Does Mineralocorticoid Receptor activation by cortisol cause ATP release and COVID-19 complications?
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