Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Vascular Pharmacology |
| Vol/bind | 52 |
| Udgave nummer | 1-2 |
| Sider (fra-til) | 70-6 |
| Antal sider | 6 |
| ISSN | 1537-1891 |
| DOI | |
| Status | Udgivet - 2009 |
Bibliografisk note
2009 Elsevier Inc. All rights reserved.Adgang til dokumentet
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Human urotensin II in internal mammary and radial arteries of patients undergoing coronary surgery. / Chen, Zhi-Wu; Yang, Qin; Huang, Yu; Fan, Li; Li, Xian-Wu; He, Guo-Wei.
I: Vascular Pharmacology, Bind 52, Nr. 1-2, 2009, s. 70-6.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Human urotensin II in internal mammary and radial arteries of patients undergoing coronary surgery
AU - Chen, Zhi-Wu
AU - Yang, Qin
AU - Huang, Yu
AU - Fan, Li
AU - Li, Xian-Wu
AU - He, Guo-Wei
N1 - 2009 Elsevier Inc. All rights reserved.
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
U2 - 10.1016/j.vph.2009.11.003
DO - 10.1016/j.vph.2009.11.003
M3 - Journal article
C2 - 19962453
VL - 52
SP - 70
EP - 76
JO - Vascular Pharmacology
JF - Vascular Pharmacology
SN - 1537-1891
IS - 1-2
ER -