Human urotensin II in internal mammary and radial arteries of patients undergoing coronary surgery

Abstract

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 p D 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 (p D 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 (p D 2:8.39 ± 0.43, E max:56.1 ± 4.0%) and RA (p D 2:9.03 ± 0.46, E max:65.2 ± 7.1%). The relaxation was abolished by endothelium denudation and by indomethacin, oxadiazoloquinoxalinone or N ω-nitro- l-arginine, oxyhemoglobin, and Ca 2+-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.