Recently, the cloning of a novel preprotachykinin gene (PPT-C) has been reported. This gene codes for a novel peptide named hemokinin 1 (HK-1). In contrast with the known tachykinins, which are exclusively expressed in neuronal tissues, PPT-C mRNA was detected primarily in hematopoietic cells. In this study, we pharmacologically characterised the effects of HK-1 using three tachykinin monoreceptor systems, namely the rabbit jugular vein (rbJV) for NK 1, the rabbit pulmonary artery (rbPA) for NK 2, and rat portal vein (rPV) for NK 3 receptors. In all these preparations substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) elicited concentration dependent contractions showing similar maximal effects and the following rank order of potency: SP > NKA = NKB in the rbJV, NKA > NKB ≫ SP in the rbPA, and NKB > NKA > SP in the rPV. In those vessels HK-1 behaved as a full agonist displaying potencies similar (rbPA and rPV) or slightly higher (rbJV) than those of SP. In the rbJV, SR 140333, a selective NK 1 receptor antagonist, antagonised the effects of HK-1 and SP with similar high potencies (pK B 9.3 and 9.5, respectively). Similar results were obtained with the pseudopeptide NK 1 antagonist, MEN 11467 (pK B 8.8 and 8.6, respectively). Taken together, these data indicate that HK-1 behaves as a NK 1 preferring receptor agonist.