Acidic and basic fibroblast growth factors dilate arterioles of
skeletal muscle through a no-dependent mechanism.
Wu, H. Mac, Yuan Yuan, Maureen McCarthy, and Harris J. Granger.
Microcirculation Research Institute and Departments of Medical
Physiology and Surgery, Texas A & M University Health Science
Center, 1901 South First Street, Building 4, Temple, TX 76504
APStracts 3:0087H, 1996.
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 utilizing isolated arterioles and intact
cremaster muscles of the rat. 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 FGF-induced vasodilation
and hyperemia. These results suggest that fibroblast growth factors
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.
Received 10 January 1996; accepted in final form 16 February
1996.
APS Manuscript Number H11-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96