Sepsis, with its consistently high morbidity and mortality rates, is a common cause of death in critically ill patients. Sepsis inflicts harm on vascular endothelial cells (VEC), resulting in endothelial dysfunction (ED). This dysfunction creates an imbalance among numerous vasodilatory and vasoconstrictive factors, manifesting as ongoing hypotension in the organism and eventually advancing to septic shock. Endothelial‑derived vasoactive factors such as nitric oxide (NO), prostaglandins (PG), endothelium‑derived hyperpolarizing factor (EDHF), endothelin (ET), angiotensin, and thromboxane all exhibit varying degrees of increase, ultimately leading to a predominant role of vasodilatory factors that promote the occurrence of septic shock. This review summarizes the mechanism related to septic shock caused by ED, focusing on the vasodilatory and vasoconstrictive factors secreted by VEC in the context of sepsis.