Journal of Clinical Research and Pharmacy

Journal of Clinical Research and Pharmacy 44 7897 074717

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The epidemic thanks to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has been spreading globally, raising increasing concerns. during this scenario, decisions on preventive, symptomatic and potentially life-saving treatments both within the general population and in patients with novel coronavirus disease 2019 (COVID-19) must be supported sound scientific evidence.

Controversial hypotheses about the possible detrimental/protective effects of antihypertensive drugs working on the renin–angiotensin–aldosterone system (RAAS) in patients with COVID-19 are postulated in several editorials and letters.
 

Through the regulation of vascular peripheral resistance and, potentially, of blood volume, the RAAS plays an important role within the etiology of hypertension. Moreover, this technique promotes atherogenic processes by increasing oxidative stress, stimulating vascular muscle and monocyte proliferation. supported their biological target, drugs inhibiting the RAAS could also be distinguished as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs) and direct renin inhibitors (DRIs). ACEIs enact their blood pressure-lowering effects by blocking the peptidyl-dipeptidase that hydrolyzes angiotensin I (A-I) to angiotensin II (A-II). additionally , it inactivates bradykinin, a vasodilating peptide promoting the discharge of nitrogen monoxide and prostacyclin. ARBs haven't any effect on bradykinin metabolism and block the consequences of A-II more selectively than ACEIs. In detail, ARBs determine their antihypertensive effect by preventing the binding of A-II to the A-II receptor type 1 (AT1). Finally, DRIs exert blood pressure-lowering effects by decreasing plasma renin activity and inhibiting the conversion of angiotensinogen to A-I .

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