Hemostasis begins with a vascular spasm, also known as the vascular phase. It starts immediately after any damage to a blood vessel, causing a sudden reduction in its diameter to minimize blood loss. After an injury, the damaged smooth muscles in the walls of the blood vessel induce a local myogenic spasm. This muscle contraction initiates the process of vasoconstriction, which is facilitated by the endothelial cells. These cells lining the inner surface of the blood vessels release various substances like adenosine diphosphate, tissue factor, prostacyclin, and peptide hormones such as endothelins. These act as local vasoconstrictors, stimulating smooth muscle contraction and reducing the lumen diameter. Additionally, the exposed endothelial cell membranes become slightly sticky and can act as temporary sealants to hold the opposite ends of the cut. Together, these mechanisms make the spasm effectively constrict the blood vessel and limit blood flow from the wound for about 20-30 mins. The vascular phase prepares the injury site for platelet adhesion, setting the stage for the subsequent phases of hemostasis.