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

AimsInternal 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.MethodsIMA and RA taken from patients undergoing coronary bypass surgery were studied in organ baths. Urotensin receptor expression was determined by RT-PCR.ResultshU-II contracted IMA with pD2 of 8.57 ± 0.41 and 45.4 ± 9.1% Emax of contraction to 100 mM KCl, whereas caused less contractile responses in RA (pD2:8.30 ± 0.79, Emax:20.4 ± 4.8%, p < 0.05). Nifedipine inhibited hU-II-contraction in IMA. In U46619-precontraction, hU-II elicited comparable relaxation in IMA (pD2:8.39 ± 0.43, Emax:56.1 ± 4.0%) and RA (pD2:9.03 ± 0.46, Emax:65.2 ± 7.1%). The relaxation was abolished by endothelium denudation and by indomethacin, oxadiazoloquinoxalinone or Nω-nitro-l-arginine, oxyhemoglobin, and Ca2+-activated K+ channel (KCa) blockers. Urotensin receptor mRNA was detected in both arteries.ConclusionshU-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 KCa activation. The relaxant response of endothelium-intact IMA and RA to hU-II demonstrates the importance of preservation of endothelium in these grafts.

Figure optionsDownload as PowerPoint slide