While brain kinin B 1 receptor (B 1 R) is virtually absent in control rats, it contributes to hypertension via a midbrain dopaminergic (DA) mechanism in spontaneously hypertensive rat (SHR) and Angiotensin II (Ang II)-induced hypertension. This study aims at determining whether B 1 R can also affect stereotypic nocifensive behavior through DA and/or other neuromediators in the same models. The selective B 1 R agonist Sar[D-Phe 8 ][des-Arg 9 ]BK was injected i.c.v. (1μg/site) to freely behaving SHR (16 weeks), Ang II-hypertensive rats (200ng/kg/min×2 weeks, s.c.) and control Wistar-Kyoto rats (WKY). Behavioral activity to the agonist was measured before and after treatment with receptor antagonists (10μg/site i.c.v. or otherwise stated) for B 1 (SSR240612), tachykinin NK 1 (RP67580), glutamate NMDA (DL-AP5), DA D 1 (SCH23390, 0.2mg/kg s.c.) and D 2 (Raclopride, 0.16mg/kg s.c.). Other studies included inhibitors (10μg/site) of NOS (l-NNA) and iNOS (1400W). The possible desensitisation of B 1 R upon repeated intracerebral stimulation was also excluded. B 1 R expression was measured by qRT-PCR in selected areas and by immunohistochemistry in the ventral tegmental area. Results showed that the B 1 R agonist had no effect in WKY, yet it induced nocifensive behavioral manifestations in both models of hypertension (face washing, sniffing, head scratching, rearing, teeth chattering, grooming, digging, licking, wet-dog shakes). These responses were prevented by all antagonists and inhibitors tested, but 1400W had a less inhibitory effect on most behaviors. Compared with WKY, B 1 R mRNA levels were markedly enhanced in hypothalamus, ventral tegmental area and nucleus accumbens of SHR and Ang II-treated rats. B 1 R was detected on DA neuron of the ventral tegmental area in SHR. Data suggest that kinin B 1 R is upregulated in midbrain DA system in hypertensive rats and its i.c.v. activation induced stereotypic nocifensive behavior that is mediated by several mediators, notably substance P, glutamate, DA and NO.