THE ROLE OF ANGIOTENSIN -2 IN THE PATHOGENESIS OF SEPTIC SHOCK DURING MULTIORGAN DYSFUNCTION SYNDROME (REVIEW)

Abstract

Septic shock is an acute pathophysiological condition characterized by vasodilation, hypotension, decreased circulating blood volume, tissue hypoxia, organ failure, and high lethality. The causes of septic vasodilation, which can lead to vascular smooth muscle dysfunction or selective vasomotor imbalance, remain controversial. In septic vasodilation, optimal pharmacological intervention is needed. Expected vascular response to shock when various vasoconstrictors are used, requires further study of the therapeutic potential of these agents. Because of all the above, it is of great interest to study and compare the therapeutic effects of angiotensin-2 and already used catecholamine and non-catecholamine vasoconstrictors in the treatment of septic shock. Angiotensin 2, approved by the FDA in 2018, is the newest available vasopressor for the treatment of vasodilatory shock. In the setting of high-dose vasopressors, exogenously administered synthetic angiotensin 2 significantly improved mean arterial pressure, decreased background vasopressor dose, and lowered sequential organ failure assessment scores in patients with refractory septic shock, In the review, the role of angiotensin-2 and its correlation with markers of sepsis for adequate management of septic shock-induced multiorgan dysfunction and arterial hypotension with ACE inhibitors is evaluated.