Document Detail


Acidic and basic FGFs dilate arterioles of skeletal muscle through a NO-dependent mechanism.
MedLine Citation:
PMID:  8853345     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fibroblast growth factors (FGFs) have been known to be potent stimulators of vascular endothelial cell proliferation and angiogenesis. Recent experimental evidence indicates that basic FGF (bFGF) is also involved in modulation of arterial pressure. In this study, we investigated the effects of acidic FGF (aFGF) and bFGF on muscle microcirculation using isolated arterioles and intact cremaster muscles of the at. In isolated microvessels, aFGF and bFGF (10(-12)-10(-8) M) significantly increased arteriolar diameter in a dose-dependent and time-dependent manner. This effect was abolished during inhibition of nitric oxide synthesis by NG-monomethyl-L-arginine (L-NMMA, 10(-4) M) but was not affected by indomethacin (10(-4) M), an inhibitor of the cyclooxygenase pathway of arachidonic acid metabolism. The vasodilation induced by FGFs was not observed in endothelium-denuded vessels. Furthermore, we studied microvascular hemodynamics in response to the growth factors in the cremaster muscle using intravital microscopy. Both aFGF and bFGF dilated arterioles of the intact cremaster muscle in a pattern similar to that observed in the isolated arterioles. At a concentration of 10(-10) M, aFGF caused a 19% increase in vessel diameter and 56% increase in blood flow. Administration of L-NMMA blocked by FGF-induced vasodilation and hyperemia. These results suggest that FGFs modulate blood flow in the skeletal muscle by acting on the endothelium of arterioles. The signaling mechanism of FGF-induced vasodilation involves the synthesis of nitric oxide by arteriolar endothelium.
Authors:
H M Wu; Y Yuan; M McCarthy; H J Granger
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  271     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1996 Sep 
Date Detail:
Created Date:  1996-12-05     Completed Date:  1996-12-05     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1087-93     Citation Subset:  IM    
Affiliation:
Microcirculation Research Institute, Texas A & M University Health Science Center, Temple 76504, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterioles / drug effects
Cyclooxygenase Inhibitors / pharmacology
Endothelium, Vascular / physiology
Fibroblast Growth Factor 1 / pharmacology*
Fibroblast Growth Factor 2 / pharmacology*
Male
Microcirculation / drug effects
Muscle, Skeletal / blood supply*
Nitric Oxide / antagonists & inhibitors,  physiology*
Rats
Rats, Sprague-Dawley
Vasodilator Agents / pharmacology*
Grant Support
ID/Acronym/Agency:
HL-21498/HL/NHLBI NIH HHS; HL-52221/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 103107-01-3/Fibroblast Growth Factor 2; 104781-85-3/Fibroblast Growth Factor 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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