| 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 |
Related Documents
:
|
18664627 - Neuropilin-1 in regulation of vegf-induced activation of p38mapk and endothelial cell o... 12446667 - Vascular endothelial growth factor modulates the transendothelial migration of mda-mb-2... 17692037 - Microvascular theory of exercise-induced bronchoconstriction in asthma: potential impli... 16674307 - Localized angiogenesis induced by human vascular endothelial growth factor-activated pl... 22739727 - Small interfering rna-mediated downregulation of beta-catenin inhibits invasion and mig... 19883077 - Cibr effectively targets nanoparticles to lfa-1 on acute lymphoblastic t cells. |
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. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| 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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Lipoprotein(a) interactions with lipid and nonlipid risk factors in early familial coronary artery d...
Next Document: Long-term probucol treatment reverses the severity of myocardial injury in watanabe heritable hyperl...