Introduction
The recent Coronavirus Disease (COVID-19) pandemic that had emerged during the last week of December 2019 in Wuhan, China and spread quickly among 210 countries with more than 2.5 million affected with a mortality of approximately 3·7% (WHO et al.,2020). COVID-19 is classified in three segments according to the clinical features; mild, moderate and severe. The data from around the world suggests that patients with specific co-morbidities like hypertension, diabetes, COPD, cardiovascular disease or kidney problems are mostly affected and have poor clinical outcomes. It can be stated that the patients with multiple complications are worst affected (Guan et al., 2020).
There is a renewed interest in the Renin-angiotensin system (RAS) amidst the ongoing pandemic of SARS-CoV2 infections or the Coronavirus Disease-19 (COVID-19). The novel coronavirus (SARS-CoV2) enters the human body through interaction of the viral Spike protein with the host ACE2 receptor, which is associated with down regulation of ACE2. On the contrary, present data have shown that hypertensive patients treated with (ACE inhibitors) ACEI/ARB (Angiotensin II receptor blockers) have elevated expression of ACE2 (Focosi et al., 2020; Ferreario et al., 2005; Furuhashi et al., 2015). Thus questions arise on whether the use of ACEI or ARBs in the hypertensive patients or patients with other comorbidities has any impact in treating COVID-19? or should the COVID-19 infected individuals continue taking these drugs, because discontinuation of these drugs may be associated with worsening of the hypertensive co-morbidity.
RAS has primarily regulatory role in cardiovascular physiology and pathology (Kuba et al., 2006). Angiotensinogen, the renin substrate, is hydrolyzed by renin to form decapeptide angiotensin I (ANG I, Figure 1). Angiotensin-converting enzyme (ACE) is responsible for converting ANG I to octapeptide angiotensin II (ANG II), which binds to angiotensin II receptor 1 (AT1R) and causes multiple biological functions such as vasoconstriction and vascular remodeling. Inhibition of ACE through ACE blockers results in partial inhibition of the formation of ANG II. ACE2, a homologue of ACE, hydrolyzes a single amino acid residue from ANG I to form angiotensin-(1–9) (WHO et al., 2020) and also can convert ANG II to vasodilator heptapeptide angiotensin-(1–7) through elimination of single residue phenylalanine. ACE2 and ACE jointly regulates vasodilator and vasoconstrictor functions to maintain the homeostasis of blood pressure. Both ACE and ACE2 are mainly found in lung, kidney, heart, pancreas and blood vessel tissue. Studies have shown that ACE2 protects from lung injury and reduce the risk of pneumonia (Imai et al., 2005; Henry et al., 2018).ACE inhibitors (ACEI, such as captopril, lisinopril, enalapril etc) or AT1R blockers (ARB, such as valsartan, losartan, telmisartan, olmesartan etc.) exhibits beneficial effect for the treatment of hypertension.