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Cardiovascular Research 2001 52(3):462-467; doi:10.1016/S0008-6363(01)00390-X
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

U-46619-induced potentiation of noradrenergic constriction in the human saphenous vein: antagonism by thromboxane receptor blockade

José M Vilaa,*, Juan B Martínez-Leónb, Pascual Medinaa, Gloria Segarraa, Rosa M Ballestera, Eduardo Oterob and Salvador Llucha

aDepartment of Physiology, University of Valencia School of Medicine, 46010 Valencia, Spain
bDepartment of Surgery, University of Valencia School of Medicine, 46010 Valencia, Spain

vila{at}post.uv.es

* Corresponding author. Departamento de Fisiología, Facultad de Medicina y Odontología, Blasco Ibáñez 17, 46010 Valencia, Spain. Tel.: +34-6-386-4644; fax: 34-6-386-4642

Objective: We investigated the potentiating effect of U-46619, a synthetic analogue of thromboxane A2 (TXA2), on the adrenergic responses in human saphenous vein. Methods: Saphenous vein rings were obtained from 35 patients undergoing coronary artery bypass surgery. The rings were suspended in organ bath chambers for isometric recording of tension. Results: U-46619 (10–10–3x10–7 mol/l) produced concentration-dependent and endothelium-independent contractile responses. U-46619 (10–10 mol/l) potentiated the contractions elicited by electrical stimulation and potassium chloride, and produced leftward shifts of the concentration–response curve for noradrenaline. The TXA2 receptor antagonist SQ-30741 (10–8 mol/l) prevented the potentiation evoked by U-46619. The dihydropyridine calcium antagonist nifedipine (10–6 mol/l) did not affect the potentiation of electrical stimulation and noradrenaline induced by U-46619, but abolished the potentiation of U-46619 on KCl-induced contractions. Conclusions: U-46619 facilitates sympathetic neurotransmission and potentiates constrictor effects of noradrenaline in human saphenous veins through stimulation of TXA2 receptors. These effects are independent of calcium entry through dihydropyridine calcium channels.

KEYWORDS Adrenergic (ant)agonists; Ca-channel; Receptors; Vasoconstriction/dilation; Veins; Endothelial factors; Vasoactive agents


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