Angiogenesis pp 101-108 | Cite as

Insights into the Vasodilation of Rat Retinal Vessels Evoked by Vascular Endothelial Growth Factor121 (VEGF121)

  • H.M. Hasséssian
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 476)


We have previously reported that cultured retinal capillary endothelial cells express VEGFR-2, whereas VEGFR-1 protein could not be detected (Hasséssian, 1997). Both types of VEGF receptor are tyrosine kinases (Ferrara and Davis-Smyth, 1997). Furthermore, we have demonstrated that VEGF121 is more potent than VEGF?65 to evoke vasodilation in the retina, and that the VEGF121 evoked vasodilation is due to the release of nitric oxide (NO) as well as prostacyclin from the endothelium (Hasséssian et al, 1998). Concurrent with the vasodilator effect, we observed increases of intracellular Ca2+, in endothelial cells, which were almost entirely due to influx across the plasma membrane (Hasséssian, 1997). Both VEGF?65 and VEGF12? were found to evoke Ca2+ influx (Hasséssian, 1997). We initiated the current set of experiments to determine if the Ca2+ influx is necessary for the vasodilator response to VEGF121 and to investigate further the cellular mechanisms responsible for the vasodilation.


Cholera Toxin Vessel Diameter Pertussis Toxin Retinal Vessel Dependent Vasodilation 
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© Springer Science+Business Media New York 2000

Authors and Affiliations

  • H.M. Hasséssian
    • 1
  1. 1.Department of Ophthalmology, Université de MontréalCentre de Recherche Guy-Bernier, Hôpital Maisonneuve-RosemontCanada

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