Vasoconstriction is caused by several regulatory molecules. Which pair correctly represents mediators of vasoconstriction?

Vasoconstriction is caused by several regulatory molecules. Which pair correctly represents mediators of vasoconstriction?

• A. Fibrinogen and vWF
• B. ADP and EPI
• C. Thromboxane A2 and Serotonin
• D. Collagen and Actomyosin

Answer: (C)

Vasoconstriction at the site of vascular injury is driven by mediators released when platelets are activated. The best pair here consists of Thromboxane A2 and Serotonin. Thromboxane A2 is produced by activated platelets and directly acts on vascular smooth muscle to cause contraction, helping narrow the vessel and reduce bleeding. Serotonin, also released from platelets, binds to receptors on smooth muscle and promotes vasoconstriction, especially in arterioles. The other options don’t fit as vasoconstrictors in this context. Fibrinogen and vWF are mainly involved in platelet adhesion and aggregation and stabilizing the plug, not constricting vessels. ADP is a platelet activator that promotes aggregation rather than vasoconstriction, and while epinephrine can cause vasoconstriction systemically, it is not a primary mediator of platelet-driven vasoconstriction in the local hemostatic response. Collagen initiates platelet adhesion, and actomyosin is a muscle protein involved in contraction, not a circulating vasoconstrictor mediator.

Vasoconstriction at the site of vascular injury is driven by mediators released when platelets are activated. The best pair here consists of Thromboxane A2 and Serotonin. Thromboxane A2 is produced by activated platelets and directly acts on vascular smooth muscle to cause contraction, helping narrow the vessel and reduce bleeding. Serotonin, also released from platelets, binds to receptors on smooth muscle and promotes vasoconstriction, especially in arterioles.

The other options don’t fit as vasoconstrictors in this context. Fibrinogen and vWF are mainly involved in platelet adhesion and aggregation and stabilizing the plug, not constricting vessels. ADP is a platelet activator that promotes aggregation rather than vasoconstriction, and while epinephrine can cause vasoconstriction systemically, it is not a primary mediator of platelet-driven vasoconstriction in the local hemostatic response. Collagen initiates platelet adhesion, and actomyosin is a muscle protein involved in contraction, not a circulating vasoconstrictor mediator.