The role for transient receptor potential channels (TRPCs) in vascular contractility are unclear. This study examines the effects of the non-specific TRPV inhibitor ruthenium red (RuRed) and the TRPV1-specific antagonist capsazepine (Cap) in isolated pressurised rat mesenteric arteries. Mesenteric arteries were dissected from male Wistar rats. Arteries were pressurised to 60mmHg and checked for leaks. The inner diameter and wall thickness was continually monitored using a video dimension analyser. The effects of RuRed (10 μM) and Cap (30 μM) and RuRed + Cap on responses to: (1) changes in intravascular pressure (myogenicity; 20, 40, 60, 80, 100 and 120mmHg); (2) phenylephrine (10 nM-0.1 mM); and (3) 60 mM KCl were studied. Time control responses were examined in separate groups. The mean diameter (± SEM) of vessels (n=18) used was 214 ± 0.4μm. In vessels which developed myogenic tone Cap alone (n=3) increased active (myogenic) diameter (P<0.05, paired t test) at 80mmHg (182 ± 3 μm) when compared to control (160 ± 3 μm). This was not further increased by addition of RuRed. However, in a separate group addition of RuRed alone (n=3) significantly increased (P< 0.05, paired t test) myogenic diameter at 80mmHg (206 ± 1 μm) compared to control (170 ± 2 μm). The mean maximum change (± SEM) in diameter (Δmax) to phenylephrine (n=3) in the presence of Cap (89 ± 1 μm) was significantly reduced (P < 0.05, paired t test) compared to that obtained in controls (136 ± 2 μm). This was further reduced by the addition of RuRed (8 ± 1 μm) (P < 0.05, paired t test) compared to that obtained in the controls and in the presence of Cap alone. EC₅₀s in the presence of Cap (1.4 μM) and both Cap and RuRed (2.9 μM) were not significantly different from control (1.3 μM). The EC₅₀ in the presence of RuRed (n=2) (1.2 μM) was significantly different (P < 0.05, paired t test) from control (0.6 μM); however, there was no significant difference in maximal response. Cap had no significant effect on the mean reduction (± SEM) in diameter to KCl (n=3) (25 ± 2 μm) compared to control (42 ± 1 μm). This was further reduced by addition of RuRed (4 ± 1 μm) (P < 0.05 compared to control). RuRed alone (n=2) again produced a reduction (84 ± 3 μm) which was significantly less (P < 0.05, paired t test) than control (112 ± 3 μm). The current study suggests that that TRPV1 channels are involved in the myogenic response of pressurised rat mesenteric arteries and in responses to phenylephrine- and KCl-induced tension. Further study is required to elucidate the roles of other TRPV channels.