AIMS: Internal mammary (IMA) and radial artery (RA) have different incidence of vasospasm and long-term patency rates in arterial grafting. We compared the vasoreactivity of human urotensin II (hU-II) and its receptor with mechanism investigations in IMA and RA. METHODS: IMA and RA taken from patients undergoing coronary bypass surgery were studied in organ baths. Urotensin receptor expression was determined by RT-PCR. RESULTS: hU-II contracted IMA with pD(2) of 8.57+/-0.41 and 45.4+/-9.1% E(max) of contraction to 100 mM KCl, whereas caused less contractile responses in RA (pD(2):8.30+/-0.79, E(max):20.4+/-4.8%, p<0.05). Nifedipine inhibited hU-II-contraction in IMA. In U(46619)-precontraction, hU-II elicited comparable relaxation in IMA (pD(2):8.39+/-0.43, E(max):56.1+/-4.0%) and RA (pD(2):9.03+/-0.46, E(max):65.2+/-7.1%). The relaxation was abolished by endothelium denudation and by indomethacin, oxadiazoloquinoxalinone or N(omega)-nitro-L-arginine, oxyhemoglobin, and Ca2+-activated K+ channel (K(Ca)) blockers. Urotensin receptor mRNA was detected in both arteries. CONCLUSIONS: hU-II is an important spasmogen in arterial grafts with receptors expressed in IMA and RA. hU-II elicits stronger contraction in IMA than in RA and a moderate endothelium-dependent relaxation attributable to nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor with involvement of K(Ca) activation. The relaxant response of endothelium-intact IMA and RA to hU-II demonstrates the importance of preservation of endothelium in these grafts.