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Endothelium‐Dependent and‐Independent Coronary Relaxation Induced by Urocortin
Author(s) -
Yao Xiaoqiang,
He GuoWei,
Chan Franky Leung,
Lau ChiWai,
Tsang SukYing,
Chen ZhenYu,
Huang Yu
Publication year - 2001
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.2001.tb01156.x
Subject(s) - urocortin , endothelium , nitric oxide , medicine , endocrinology , nitric oxide synthase , receptor
A bstract Urocortin, a newly identified polypeptide, possesses cardiac effects. However, the underlying mechanism of its coronary action is still unclear. In the present study we investigated the possible role of endothelial nitric oxide and Ba 2+ ‐sensitive K + channels in the endothelium‐dependent relaxant response to urocortin in the isolated rat left anterior descending coronary arteries. Changes of vessel tone were measured in microvessel myographs. Urocortin produced both endothelium‐dependent and‐independent relaxation with IC 50 of 2.52 nM and 16.5 nM, respectively. Denuation of endothelium decreased the relaxing potency of urocortin. In the endothelium‐intact rings pretreated with 100 μM N G ‐nitro‐L‐arginine methyl ester (L‐NAME) or 10 μM 1H‐[1,2,4]oxadiazolo[4,2‐α]quinoxalin‐1‐one (ODQ), the urocortin‐induced relaxation was similar to that observed in endothelium‐denuded rings. The relaxant response to urocortin was markedly reduced in endothelium‐intact rings precon‐stricted by 35 mM K + . Pretreatment with 100 μM BaCI 2 significantly reduced urocortin‐induced relaxation without an effect on the maximum relaxation. Combined treatment with BaCI 2 plus L‐NAME did not produce additive inhibition. In contrast, BaCI 2 did not alter urocortin‐induced relaxation in the endothelium‐denuded rings. In the endothelium‐denuded rings, BaCI 2 at 100 μM also inhibited nitric oxide donor‐induced relaxation. In conclusion, our results suggest that urocortin‐induced endothelium‐dependent relaxation of rat coronary arteries is primarily mediated by endothelial nitric oxide and subsequent activation of Ba 2+ ‐sensitive K + channels. The urocortin‐induced endothelium‐dependent relaxation appears to be cyclic GMP‐dependent.