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Cardiovascular Research 1997 36(2):276-281; doi:10.1016/S0008-6363(97)00177-6
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Activation of Flk-1/KDR mediates angiogenesis but not hypotension

Bernard Malavauda,b, Ivan Tackc, Frédéric Joncaa,b, Françoise Praddaudec, Françoise Moroa, Jean-Louis Aderc and Jean Plouëta,*

aLaboratoire de Biologie Moléculaire Eucaryote/UPR CNRS 9006, 118 route de Narbonne, 31062 Toulouse Cedex, France
bService d'Urologie, CHU Purpan — Faculté de Médecine, 31062 Toulouse Cedex, France
cLaboratoire de Physiologie/Unité INSERM 388 31062 Toulouse Cedex, France

* Corresponding author. Tel. (+33–5) 61335826; Fax (+33–5) 61335886.

Objective: The concept of therapeutic angiogenesis with vascular endothelial growth factor (VEGF) has been validated in peripheral arterial disease. Its use in myocardial ischemia may be delayed as the result of the description in a porcine model of peripheral vasodilation after intraluminal injections of VEGF resulting in a 50% fatality rate by hypotension. We carried out this study to test whether VEGF-induced hypotension (1) is species specific, (2) is mediated by the receptor mediating angiogenesis, (3) is prevented by inhibition of nitric oxide synthase. Methods: In the rabbit corneal pocket assay we tested whether a previously published anti-idiotypic antibody (AIA) agonist of the VEGF receptor Flk-1/KDR could elicit angiogenesis. Various doses of recombinant VEGF or AIA were injected into anesthetized normotensive Wistar–Kyoto rats and the mean arterial blood pressure (MABP) was recorded. To test the implication of nitric oxide in VEGF-induced hypotension we treated the animals with a competitive inhibitor of nitric oxide synthase prior to the injection of VEGF. Results: Both VEGF and AIA induce angiogenesis but only intravenous injections of VEGF induced a rapid, transient and dose-dependent decrease in MABP. The ED50 was 0.5 µg. The interval between two VEGF injections required to lead to a decrease of MABP was 40 minutes. Nitric oxide synthesis inhibitor prevented, in a reversible fashion, the effect of VEGF. Conclusion: VEGF-induced hypotension is not species specific. It is prevented by nitric oxide inhibition. VEGF-induced angiogenesis and hypotension are not mediated in vivo by the same VEGF receptor

KEYWORDS Angiogenesis; Blood pressure; Vascular endothelial growth factor; Flk-1/KDR; Flt-1; Nitric oxide; Wistar–Kyoto rat; Rabbit


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