(Circulation. 1997;95:1030-1037.)
© 1997 American Heart Association, Inc.
Articles |
Vascular Endothelial Growth Factor/Vascular Permeability Factor Augments Nitric Oxide Release From Quiescent Rabbit and Human Vascular Endothelium
the Departments of Biomedical Research and Medicine (Cardiology), St Elizabeth's Medical Center, Tufts University, School of Medicine, Boston, Mass. Current address for Dr van der Zee is Department of Cardiology, Academic Hospital Maastrict, Maastrict, Netherlands.
Correspondence to Jeffrey M. Isner, MD, St Elizabeth's Medical Center, 736 Cambridge St, Boston MA 02135-2997. E-mail vejeff@aol.com.
Background Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF) is an endothelial cell (EC) mitogen. This feature is considered central to the documented role of VEGF/VPF in promoting angiogenesis. More recent evidence suggests that VEGF/VPF may also serve a "maintenance" function, modulating various aspects of EC biology. In the present study, we sought to determine the extent to which VEGF/VPF may stimulate the release of NO from normal ECs.
Methods and Results VEGF/VPF produced a dose-dependent rise in NO concentration ([NO]) from vascular segments of rabbit thoracic aorta, pulmonary artery, and inferior vena cava. In comparison to stimulation with acetylcholine, the onset of increased [NO] after administration of VEGF/VPF was slower, reaching a maximum value after 8 minutes. Preincubation of the aortic segments with L-arginine raised by twofold both baseline [NO] and [NO] stimulated by addition of 2.5 µg/mL VEGF/VPF. Removal of CaCl2 from the Krebs solution, disruption of the endothelium, and administration of NG-monomethyl-L-arginine abrogated the stimulatory effect of 10 µg/mL VEGF/VPF. Similar findings were documented with an NO-specific polarographic electrode to measure NO released from cultured human umbilical vein ECs.
Conclusions VEGF/VPF stimulates production of NO from rabbit and human ECs. This finding (1) constitutes inferential evidence for the presence of functional VEGF/VPF receptors on quiescent endothelium of the adult rabbit as well as human ECs and (2) supports the notion that putative maintenance functions of VEGF/VPF may include regulation of baseline synthesis and/or release of EC NO.
Key Words: endothelium-derived factors • nitric oxide • endothelium
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J. R. Horowitz, A. Rivard, R. van der Zee, M. Hariawala, D. D. Sheriff, D. D. Esakof, G. M. Chaudhry, J. F. Symes, and J. M. Isner Vascular Endothelial Growth Factor/Vascular Permeability Factor Produces Nitric Oxide–Dependent Hypotension : Evidence for a Maintenance Role in Quiescent Adult Endothelium Arterioscler Thromb Vasc Biol, November 1, 1997; 17(11): 2793 - 2800. [Abstract] [Full Text]
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Z. Luo, M. Diaco, T. Murohara, N. Ferrara, J. M. Isner, and J. F. Symes Vascular Endothelial Growth Factor Attenuates Myocardial Ischemia-Reperfusion Injury Ann. Thorac. Surg., October 1, 1997; 64(4): 993 - 998. [Abstract] [Full Text]
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