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ACE and ARB blood pressure meds (i.e losartan) and coronavirus concern
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<blockquote data-quote="tareload" data-source="post: 174762"><p><a href="http://Angiotensin%20receptor%20blockers%20as%20tentative%20SARS-CoV-2therapeutics" target="_blank">https://onlinelibrary.wiley.com/doi/epdf/10.1002/ddr.21656</a></p><p></p><p><em><span style="color: rgb(84, 172, 210)">As described above, ACE2 is the common binding site for both the SARS‐CoV of the 2002–2003 SARS epidemic and, most likely, also the SARS‐CoV‐2 strain underlying the current COVID‐19 epidemic. Hence, the suggestion to treat SARS patients with AT1R antagonists for increasing their ACE2 expression seems counter‐intuitive. However, several observations from studies on SARS‐CoV, which very likely are relevant also for SARS‐CoV‐2, seem to suggest otherwise. </span>It has been demonstrated that the binding of the coronavirus spike protein to ACE2, its cellular binding site, leads to ACE2 downregulation, which in turn results in excessive production of angiotensin by the related enzyme ACE, while less ACE2 is capable of converting it to the vasodilator heptapeptide angiotensin 1–7. This in turn contributes to lung injury, as angiotensin‐stimulated AT1R results in increased pulmonary vascular permeability, thereby mediating increased lung pathology (Imai et al., <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0015" target="_blank"> 2005</a>; Kuba et al., <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0018" target="_blank"> 2005</a>). <span style="color: rgb(84, 172, 210)">Therefore, higher ACE2 expression following chronically medicating SARS‐CoV‐2 infected patients with AT1R blockers, while seemingly paradoxical, may protect them against acute lung injury rather than putting them at higher risk to develop SARS.</span></em><span style="color: rgb(84, 172, 210)"> This may be accounted for by two complementary mechanisms: blocking the excessive angiotensin‐mediated AT1R activation caused by the viral infection, as well as upregulating ACE2, thereby reducing angiotensin production by ACE and increasing the production of the vasodilator angiotensin 1–7.</span> These aspects on the role of dysregulated ACE2 in SARS‐CoV pathogenesis are reviewed in detail by de Wit et al., <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0007" target="_blank"> 2016</a>. Incidentally, following the SARS‐CoV epidemic of 2002–2003, ACE2 inhibitors were suggested as SARS therapeutics (Huentelman et al., <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0014" target="_blank"> 2004</a>; Turner et al., <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0033" target="_blank"> 2004</a>); however, this proposal has not led to new drugs.</p></blockquote><p></p>
[QUOTE="tareload, post: 174762"] [URL='http://Angiotensin%20receptor%20blockers%20as%20tentative%20SARS-CoV-2therapeutics']https://onlinelibrary.wiley.com/doi/epdf/10.1002/ddr.21656[/URL] [I][COLOR=rgb(84, 172, 210)]As described above, ACE2 is the common binding site for both the SARS‐CoV of the 2002–2003 SARS epidemic and, most likely, also the SARS‐CoV‐2 strain underlying the current COVID‐19 epidemic. Hence, the suggestion to treat SARS patients with AT1R antagonists for increasing their ACE2 expression seems counter‐intuitive. However, several observations from studies on SARS‐CoV, which very likely are relevant also for SARS‐CoV‐2, seem to suggest otherwise. [/COLOR]It has been demonstrated that the binding of the coronavirus spike protein to ACE2, its cellular binding site, leads to ACE2 downregulation, which in turn results in excessive production of angiotensin by the related enzyme ACE, while less ACE2 is capable of converting it to the vasodilator heptapeptide angiotensin 1–7. This in turn contributes to lung injury, as angiotensin‐stimulated AT1R results in increased pulmonary vascular permeability, thereby mediating increased lung pathology (Imai et al., [URL='https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0015'] 2005[/URL]; Kuba et al., [URL='https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0018'] 2005[/URL]). [COLOR=rgb(84, 172, 210)]Therefore, higher ACE2 expression following chronically medicating SARS‐CoV‐2 infected patients with AT1R blockers, while seemingly paradoxical, may protect them against acute lung injury rather than putting them at higher risk to develop SARS.[/COLOR][/I][COLOR=rgb(84, 172, 210)] This may be accounted for by two complementary mechanisms: blocking the excessive angiotensin‐mediated AT1R activation caused by the viral infection, as well as upregulating ACE2, thereby reducing angiotensin production by ACE and increasing the production of the vasodilator angiotensin 1–7.[/COLOR] These aspects on the role of dysregulated ACE2 in SARS‐CoV pathogenesis are reviewed in detail by de Wit et al., [URL='https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0007'] 2016[/URL]. Incidentally, following the SARS‐CoV epidemic of 2002–2003, ACE2 inhibitors were suggested as SARS therapeutics (Huentelman et al., [URL='https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0014'] 2004[/URL]; Turner et al., [URL='https://onlinelibrary.wiley.com/doi/full/10.1002/ddr.21656#ddr21656-bib-0033'] 2004[/URL]); however, this proposal has not led to new drugs. [/QUOTE]
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ACE and ARB blood pressure meds (i.e losartan) and coronavirus concern
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