Mice previously injected intravenously with lead acetate solution were injected subcutaneously with Polymixin B Sulphate. This resulted in calcification at the latter injection site. Histological evidence showed marked mast cell degranulation, local vasodilation and the efflux of lead ions from these vessels. At twenty four hours after injection abundant calcium and phosphate ions were readily demonstrated. In addition, groups of mice pre-injected intravenously with lead acetate, were injected with constituents of mast cell granules. These included histamine phosphate, serotonin creatinine sulphate, heparin, chondroitin sulphate or hyaluronic acid. Of these exogenous constituents used, calcification was found only after serotonin and histamine injections, both of which are potent vasodilators and presumbly increase capillary permeability. It is postulated that the role of the mast cell in calcergy may be mainly that of producing local vasodilation with increased capillary permeability rather than the initial binding of metallic ions.