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. 2020 Apr-Jun;21(2):1470320320927851.
doi: 10.1177/1470320320927851.

COVID-19 and hypertension

Spoorthy Kulkarni  1 , Bernadette L Jenner  1 , Ian Wilkinson  2
Affiliations

COVID-19 and hypertension

Spoorthy Kulkarni et al. J Renin Angiotensin Aldosterone Syst. 2020 Apr-Jun.
No abstract available

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Conflict of interest statement

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Traditional RAAS pathway, presumed ACE2 pathway and sites of ACEi and ARB action are highlighted. The ACE2 pathway is thought to increase vasodilatory peptides (Ang 1–9, Ang 1–7) and decrease downstream effects of RAAS activation. ACEi might upregulate ACE2 expression. The effect of ARB use is probably slightly different from ACEi, as angiotensin II and ACE levels remain unaffected. Viral entry is thought to be via ACE2 receptor in the presence of transmembrane serine protease. RAAS: renin–angiotensin–aldosterone system; ACE: angiotensin-converting enzyme; AT1: angiotensin receptor type 1; AT2: angiotensin receptor type 2; ARB: angiotensin receptor blocker; ang: angiotensin; S: spike protein; Mas receptor: Mitochondrial assembly receptor.
Figure 2.
Figure 2.
Summary of the hypothesized unknown effects of ACEi/ARB use in patients affected by coronavirus disease 2019. Ang II: angiotensin II.
See this image and copyright information in PMC

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