Bradykinin (BK) and related kinins excite primary sensory neurons, thus leading to the activation of sensory impulses. More recently, both functional and neurochemical evidence have been accumulated that BK evokes release of neuropeptides, including calcitonin gene-related peptide and the tachykinins substance P and neurokinin A, from peripheral terminals of capsaicin-sensitive primary afferents. The present article will review the mechanisms and the pathophysiological implications of the ability of BK to release sensory neuropeptides at the peripheral level. An account of the clinical studies performed on this subject will be also given.