Zinc (Zn 2+ ) is an essential micronutrient and the second most abundant trace metal in the human body. The important role that Zn 2+ plays in haemostasis is exemplified by platelet-related bleeding phenotypes coinciding with dietary Zn 2+ deficiency. These phenotypes are rectified upon Zn 2+ supplementation. Labile (unbound) Zn 2+ is present in the plasma at micromolar levels, but is also detected in atherosclerotic plaques, and released from platelet alpha granules. Therefore, it is likely that localised Zn 2+ concentrations are higher at sites of thrombosis and haemostasis. Exogenous Zn 2+ is a regulator of the haemostatic responses, with roles during coagulation and platelet activation. Extracellular Zn 2+ gains access to the platelet cytosol and induces full platelet activation at high concentrations, and potentiates platelets to activation by conventional agonists at lower concentrations. Zn 2+ -induced platelet activation is dependent on PKC and integrin α IIb β 3 , and is associated with tyrosine phosphorylation of platelet proteins. Agonist evoked platelet activation results in intracellular Zn 2+ ([Zn 2+ ] i ) fluctuations that are sensitive to the platelet redox state. Increases in [Zn 2+ ] i correlate with activation responses, including shape change, granule release, α IIb β 3 activation and phosphatidylserine exposure, consistent with a role as a second messenger. This review provides insight into the numerous demonstrated and potential roles for Zn 2+ in platelet function during thrombosis and haemostasis, highlighting its increasing acceptance as an intracellular and extracellular platelet regulatory agent.