**9. Link between coronavirus and RAAS**

RAAS is the neurohormonal pathway that controls blood pressure and fluid balance. The mechanism of the rennin angiotensin is the formation of angiotensin 2, a vasoactive hormone attached to the receptor of the type I angiotensin, which is present in the renal, cardiac, and respiratory systems. It has a vital role in causing the hypertrophy of the myocardium and fibrosis. Further, it causes inflammation, remodeling of vascular endothelium, and formation of atherosclerosis plaque. The Angiotensin-converting enzyme 2 is present in human body tissues, and it affects the mechanism of angiotensin II and the reducing of vasoconstriction effect [29].

SARS-CoV-2 connected to the ACE2 receptor by releasing the spikes protein into host cells causes the regulation of ACE2 and bringing about the local aggregation of angiotensin II. Respiratory severe illness is a sign of COVID-19 and an essential reason for morbidity and mortality; RAAS is proposed to cause an extreme lung injury. Angiotensin-converting enzyme II is considered as the entry for SARS-CoV-2.

The entry of COVID-19 infection in the human body occurs if the virus comes in contact with the angiotensin-converting enzyme II cell surface. This enzyme acts with SARS-CoV-2 by restricting the receptor binding space of the viral spike protein. In the human lung, type II alveolar epithelial cells, ACE2 and transmembrane protease serine III are viewed as fundamentally liable for virus entry in COVID-19 [29].

### **10. The possible impact of RAS inhibitors on COVID-19**

At the start of the COVID 19 episode, the patients with hypertension utilizing angiotensin-converting enzyme inhibitors might provide unfavorable results. The studies mentioned that mineral corticoid receptor antagonists (MRAs) increase the movement of angiotensin-converting enzyme II in the heart and kidney. The antihypertensive medications initiate the ACE2 increase the chances of the portal of entry for the COVID infection [30].

*Impact of Cardiovascular Diseases on the Outcome of Patients with COVID-19 DOI: http://dx.doi.org/10.5772/intechopen.101121*
