Indirect evidence has abundantly been presented to support the view that substance P (SP) is involved in the vasodilatation following activation of fine calibre pain fibres (Lembeck & Holzer 1979). In this respect, the dental pulp is interesting since it is richly supplied with SP‐immunoreactive nerves originating from the trigeminal system (Olgart et al. 1917b, Brodin et al. 1980). These nerves are in all probability related to nociception (Henry et al. 1980). Recent observations in the cat showing that electrical stimulation of the inferior alveolar nerve produces an atropine resistant vasodilatation (Gazelius & Olgart 1980), and a release of substance P‐like immunoreactivity in the pulp (Olgart et al. 1977a, Brodin et al. 1980) are in accord with the suggested role of SP. In the present study, the availability of an antagonist to SP has made possible the further elucidation of the role of SP as a mediator of antidromic vasodilatation in the dental pulp and in the oral mucosa of the cat. We have also determined whether (D‐Pro2, D‐Phe7, D‐Trp9)‐SP specifically blocks the vascular effects of SP.