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Cardiovascular Research 2002 54(3):701; doi:10.1016/S0008-6363(02)00393-0
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

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

J.Y Jeremya and D.P Mikhailidisb,*

aBristol Heart Institute, University of Bristol, Bristol BS2 8HW, UK
bDepartment of Clinical Biochemistry, Royal Free and University College Medical School, Royal Free Hospital Campus, Pond Street, London NW3 2QG, UK

* Corresponding author. Tel.: 0044-20783-02258; fax: 0044-20783-02235

Received 18 February 2002; accepted 5 March 2002

Vila et al. [1] elegantly demonstrated that thromboxane A2 (TXA2) augments adrenergic-mediated constriction of the human isolated saphenous vein, an effect blocked by a TXA2 antagonist. They also comment on the potential benefit from prostacyclin (PGI2) formation that may not be affected by highly specific TXA2 antagonists.

The relationship between TXA2 and adrenergic stimulation on the one hand and PGI2 release on the other is complex. We previously reported that both TXA2 and noradrenaline stimulates PGI2 release from isolated aortic rings, through a calcium dependent mechanism [2,3]. Noradrenaline also stimulates PGI2 formation in porcine saphenous veins [4]. The same may also be true for the human saphenous vein. We suggested that the release of PGI2 in response to TXA2 may constitute a protective response against excessive platelet adhesion, vasospasm and vascular smooth muscle cell proliferation (all promoted by TXA2 but inhibited by PGI2) [5]. These mechanisms are of particular relevance to the pathophysiology and treatment of early and late saphenous vein graft failure [5].

As more work is published we are beginning to understand the complexity of the interactions that occur between various mediators in the arterial and venous circulation. Hopefully this will lead to more targeted treatments, as Vila et al. suggest [1].


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  1. Vila J.M, Martinez-Leon J.B, Medina P, et al. U-46619-induced potentiation of noradrenergic constriction in the human saphenous vein: antagonism by thromboxane receptor blockade. Cardiovasc Res (2001) 52:462–467.[Abstract/Free Full Text]
  2. Jeremy J.Y, Mikhailidis D.P, Dandona P. Thromboxane A2 analogue (U 46619) stimulates PGI2 synthesis. Eur J Pharmacol (1985) 107:259–262.[CrossRef][Web of Science][Medline]
  3. Jeremy J.Y, Mikhailidis D.P, Dandona P. Adrenergic modulation of vascular prostacyclin (PGI2) secretion. Eur J Pharmacol (1985) 114:33–40.[CrossRef][Web of Science][Medline]
  4. Jeremy J.Y, Izzat M.B, Birkett S.D, Knight D.M, Bryan A.J, Angelini G.D. Reduced prostacyclin and increased leukotriene B4 synthesis in porcine vein grafts. Ann Thorac Surg (1996) 61:143–148.[Abstract/Free Full Text]
  5. Jeremy J.Y, Mehta D, Bryan A.J, Lewis D, Angelini G.D. Platelets and saphenous vein graft failure following coronary artery bypass graft surgery. Platelets (1997) 8:295–309.[CrossRef][Web of Science][Medline]

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