<p>The epithelial sheath covering the stingray spine results in wounds to humans that are characterized by edema, necrosis, effusive bleeding and extreme pain. Kinins are potent autocoids that produce each of these symptoms. In this study, the dorsal and ventral portions of the epithelial sheath covering the spine of the Atlantic stingray (<i>Hypanus sabinus</i>) spine were analysed for components of the kallikrein–kinin system. Colorimetric assays showed kallikrein activity in both dorsal and ventral epithelial sheath preparations. Trypsin, which cleaves the inactive proenzyme to its active (kallikrein) form, resulted in an increase in the median kallikrein of 2.02 and 0.94 in dorsal and ventral spine preparations, respectively. Radioimmunoassay of kinin itself showed detectable immunoreactivity in the entire integumentary sheath. Trypsin treatment resulted in an increase in median immunoreactivity by 12.88. <i>In vivo</i> analyses for effects of epithelial extract on mammalian capillary leakage showed an increase in median capillary leakage of 5.25 in spine epithelia-treated animals compared to controls. Components of the kallikrein–kinin system are present in the Atlantic stingray spine epithelium and may account for some of the pathologies of stings in humans.</p>