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Since the beginning of 2020, the whole world has been struggling with the pandemic of Coronavirus Disease 2019 (COVID-19) caused by a novel coronavirus SARS-CoV-2. The SARS-CoV-2 infection depends on ACE2, TMPRSS2, and CD147, which are expressed on host cells. Several studies suggest that some single nucleotide polymorphisms (SNPs) of ACE2 might be a risk factor of COVID-19 infection. Genotypes affect ACE2 structure, its serum concentration, and levels of circulating angiotensin (1-7). Moreover, there is evidence that ACE genotype affects the outcomes of acute respiratory distress syndrome (ARDS) treatment, the most severe consequence of SARS-CoV-2 infection. COVID-19 morbidity, infection course, and mortality might depend on ACE D allele frequency. The aim of this narrative review was to analyze and identify the mechanisms of ACE-I and ARBs with particular emphasis on angiotensin receptors and their polymorphism in the light of COVID-19 pandemic as these medications are commonly prescribed to elderly patients. There is no direct evidence yet for ACE-I or ARBs in the treatment of COVID-19. However, for those already taking these medications, both the European Society of Cardiology and the American College of Cardiology recommend continuing the treatment, because at present, there is no clear clinical or scientific evidence to justify the discontinuation of ACE-I or ARBs. Individualized treatment decisions should be based on the clinical condition and co-morbidities of each patient.

Adrenomedullin (ADM) is indicated to be a biologically active polypeptide released by endothelium with strong hypotensive, long-acting vasodilatator properties. It is suggested that development of preeclampsia is partly related to decreased ADM influence on blood vessels.The purpose of this study was to evaluate the adrenomedullin mRNA expression in placenta of preeclamptic women and additionally to assess the correlation between ADM mRNA expression and -1984AG ADM gene polymorphism.26 preeclamptic (PE), 20 with gestational hypertension (GH) and 43 normotensive healthy pregnant women have been involved into the study. The placenta samples were collected instantly after delivery from the central part of maternal side. The ADM gene expression was measured with the real-time polymerase chain reaction (rt-PCR). The results were standardized according to the reference glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene. The -1984AG ADM gene polymorphism was determined by PCR/RFLP assayLower expression of ADM mRNA in PE group (0.881 +/- 0.254 vs. 1.039 +/- 0.391 in controls, ns) has been investigated. In PE group the placental ADM mRNA expression was slightly higher at women carrying AA genotype (0.890 +/- 0.263 vs. 0.842 +/- 0.231, ns). In the control group higher placental ADM mRNA expression in women with AG + GG genotype of -1984AG ADM gene polymorphism (1.249 +/- 0.431) in comparison to women carrying AA genotype (1.036 +/- 0.356, ns) was observed. The study also revealed negative correlation between placental ADM mRNA expression and systolic blood pressure in hypertensive pregnant women (p = 0.020).Reduced mRNA expression for ADM in the placenta connected with reverse correlation of systolic blood pressure in preeclamptic women suggests the significant role of disturbances in placental secretion of ADM in etiology of preeclampsia.