Document Detail


Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium.
MedLine Citation:
PMID:  9409257     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In vitro studies suggest that vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) may stimulate release of nitric oxide (NO) from endothelial cells. To investigate the hemodynamic consequences of recombinant VEGF/VPF administered in vivo, recombinant human VEGF/VPF was administered as a bolus dose of 500 micrograms to anesthetized (n = 6) or conscious (n = 5) New Zealand White rabbits, as well as anesthetized rabbits with diet-induced hypercholesterolemia (HC; n = 7). Anesthetized Yorkshire farm pigs (no specific dietary pretreatment) were studied before and after receiving 500 micrograms intravenous (IV; n = 5) or intracoronary (IC; n = 5) VEGF/VPF. In anesthetized, normal rabbits, mean arterial pressure (MAP) fell by 20.5 +/- 1.4% (P < .05 versus baseline) within 3 minutes after IV VEGF/VPF. Pretreatment with N omega-nitro-L-arginine caused a significant inhibition of VEGF/VPF-induced hypotension. In conscious, normal rabbits, VEGF/VPF produced a consistent though lesser reduction in MAP. The fall in MAP induced by VEGF/VPF in anesthetized, HC rabbits (21.5 +/- 2.5% from baseline) was no different from that observed in normal anesthetized rabbits. In pigs, both IV and IC administration of VEGF/VPF produced a prompt reduction in MAP. Heart rate increased, while cardiac output, stroke volume, left atrial pressure, and total peripheral resistance all declined to a similar, statistically significant degree in both IV and IC groups. Epicardial echocardiography disclosed neither global nor segmental wall motion abnormalities in response to VEGF/VPF. We conclude that (1) VEGF/VPF-stimulated release of NO, previously suggested in vitro, occurs in vivo; (2) this finding suggests that functional VEGF/VPF receptors are present on quiescent adult endothelium, consistent with a maintenance function for VEGF/VPF, which may include regulation of NO; and (3) the preserved response of HC rabbits suggests that endothelial cell receptors for VEGF/VPF are spared in the setting of hypercholesterolemia.
Authors:
J R Horowitz; A Rivard; R van der Zee; M Hariawala; D D Sheriff; D D Esakof; G M Chaudhry; J F Symes; J M Isner
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  17     ISSN:  1079-5642     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  1997 Nov 
Date Detail:
Created Date:  1998-01-22     Completed Date:  1998-01-22     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2793-800     Citation Subset:  IM    
Affiliation:
Department of Medicine (Cardiology), St Elizabeth's Medical Center, Tufts University School of Medicine, MA, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / drug effects
Cholesterol, Dietary / toxicity
Diet, Atherogenic
Echocardiography
Endothelial Growth Factors / pharmacology,  toxicity*
Endothelium, Vascular / secretion*
Enzyme Inhibitors / pharmacology
Hemodynamics / drug effects
Humans
Hypercholesterolemia / etiology,  physiopathology
Hypotension / chemically induced*,  physiopathology
Lymphokines / pharmacology,  toxicity*
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors,  metabolism
Nitroarginine / pharmacology
Rabbits
Receptor Protein-Tyrosine Kinases / drug effects,  physiology
Receptors, Growth Factor / drug effects,  physiology
Receptors, Vascular Endothelial Growth Factor
Recombinant Proteins / pharmacology,  toxicity
Secretory Rate / drug effects
Swine
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Vasodilation / drug effects
omega-N-Methylarginine / pharmacology
Grant Support
ID/Acronym/Agency:
HL 02824/HL/NHLBI NIH HHS; HL53354/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cholesterol, Dietary; 0/Endothelial Growth Factors; 0/Enzyme Inhibitors; 0/Lymphokines; 0/Receptors, Growth Factor; 0/Recombinant Proteins; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 2149-70-4/Nitroarginine; EC 1.14.13.39/Nitric Oxide Synthase; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases; EC 2.7.10.1/Receptors, Vascular Endothelial Growth Factor

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