Original ArticleEffects of Endothelin-1 on the Relaxation of Rat Coronary ArteriesGarcía-Villalón, Angel Luis MD, PhD; Fernández, Nuria PhD, VMD; Monge, Luis MD, PhD; Salcedo, Adely MD, PhD; Diéguez, Godofredo MD, PhDAuthor Information From the Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain. Received for publication February 2, 2009; accepted July 22, 2009. Supported, in part, by Ministerio de Ciencia y Tecnologia (grants BFU2004-04054 and SAF2008-14140). The authors report no conflicts of interest. Reprints: Angel Luis García-Villalón, MD, PhD, Departamento de Fisiología Facultad de Medicina, Universidad Autonoma, Arzobispo Morcillo 2, 28029 Madrid, Spain (e-mail: email@example.com). Journal of Cardiovascular Pharmacology: November 2009 - Volume 54 - Issue 5 - p 445-450 doi: 10.1097/FJC.0b013e3181bae3f0 Buy Metrics Abstract To analyze the effects of endothelin-1 on the β-adrenergic response of the coronary circulation, 2-mm-long segments of coronary arteries from rats were prepared for isometric tension recording in organ baths. The relaxation to isoproterenol (3 × 10−8 M), field electrical stimulation (4 Hz, 0.1-millisecond duration, 10 seconds), acetylcholine (3 × 10−8 M), and sodium nitroprusside (10−9 M) was recorded in arteries precontracted with U46619 (10−7 to 5 × 10−7 M) before and after treatment with endothelin-1 (3 × 10−10 and 10−9 M). The relaxation to isoproterenol was increased by treatment with endothelin-1 and with the endothelin ETB antagonist BQ788 (10−6 M) but not with the endothelin ETA antagonist BQ123 (10−6 M) or with the blocker of protein kinase C chelerythrine (10−5 M). In the presence of BQ788, BQ123, or chelerythrine, endothelin-1 did not modify the relaxation to isoproterenol. Treatment with endothelin-1 did not modify the relaxation to electrical stimulation, acetylcholine, or sodium nitroprusside. These results suggest that endothelin-1 may potentiate coronary β-adrenergic vasodilatation, at least in part due to stimulation of endothelin ETA receptors and activation of protein kinase C. © 2009 Lippincott Williams & Wilkins, Inc.