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Titolo:
VEGF(121)- and bFGF-induced increase in collateral blood flow requires normal nitric oxide production
Autore:
Yang, HT; Yan, Z; Abraham, JA; Terjung, RL;
Indirizzi:
Univ Missouri, Coll Vet Med, Columbia, MO 65211 USA Univ Missouri Columbia MO USA 65211 Coll Vet Med, Columbia, MO 65211 USA Univ Missouri, Coll Med, Columbia, MO 65211 USA Univ Missouri Columbia MOUSA 65211 uri, Coll Med, Columbia, MO 65211 USA Univ Missouri, Dalton Cardiovasc Res Ctr, Columbia, MO 65211 USA Univ Missouri Columbia MO USA 65211 ovasc Res Ctr, Columbia, MO 65211 USA Scios Inc, Sunnyvale, CA 94086 USA Scios Inc Sunnyvale CA USA 94086Scios Inc, Sunnyvale, CA 94086 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 3, volume: 280, anno: 2001,
pagine: H1097 - H1104
SICI:
0363-6135(200103)280:3<H1097:VABIIC>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; RABBIT MODEL; IN-VIVO; LIMB ISCHEMIA; GENE-TRANSFER; ANGIOGENESIS; CELLS; PROLIFERATION; EXPRESSION; HINDLIMB;
Keywords:
angiogenesis; vascular remodeling; peripheral arterial insufficiency; microsphere; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Yang, HT Univ Missouri, Coll Vet Med, E102 Vet Med Bldg, Columbia, MO 65211 USA Univ Missouri E102 Vet Med Bldg Columbia MO USA 65211 O 65211 USA
Citazione:
H.T. Yang et al., "VEGF(121)- and bFGF-induced increase in collateral blood flow requires normal nitric oxide production", AM J P-HEAR, 280(3), 2001, pp. H1097-H1104

Abstract

The angiogenic proteins basic fibroblast growth factor (bFGF; FGF-2) and vascular endothelial growth factor 121 (VEGF(121)) are each able to enhance the collateral-dependent blood flow after bilateral femoral artery ligationin rats. To study the effect of nitric oxide (NO) synthase (NOS) inhibition on bFGF- or VEGF(121)-induced blood flow expansion, the femoral arteries of male Sprague-Dawley rats were ligated bilaterally, and the animals were given tap water [non-N-G-nitro-L-arginine methyl ester (L-NAME) group; n = 36] or water that contained L-NAME (L-NAME group; 2 mg/ml, n = 36). Animalsfrom each group were further divided into three subgroups: vehicle (n = 12), bFGF (5 mug.kg(-1).day(-1), n = 12), or VEGF(121) (10 mug.kg(-1).day(-1), n = 12). Growth factors were delivered via intra-arterial infusion with osmotic pumps over days 1-14. On day 16, after a 2-day delay to permit clearance of bFGF and VEGF from the circulation, maximal collateral blood flow was determined by Sr-85- and Ce-141-labeled microspheres during treadmill running. L-NAME (similar to 137 mg.kg(-1).day(-1)) for 18 days increased systemic blood pressure (similar to 26%, P < 0.001). In the absence of L-NAME, collateral-dependent blood flows to the calf muscles were greater in the VEGF(121)- and bFGF-treated subgroups (85 +/- 4.5 and 80 +/- 2.9 ml.min(-1).100 g(-1), respectively) than in the vehicle subgroup (49 +/- 3.0 ml.min(-1).100 g(-1), P < 0.001). In the presence of NOS inhibition by L-NAME, blood flows to the calf muscles were essentially equivalent among the three subgroups (54 +/- 3.0, 56 +/- 5.1, and 47 +/- 2.0 ml.min(-1).100 g(-1) in the bFGF-, VEGF(121)-, and vehicle-treated subgroups, respectively) and were not different from the blood flow in the non-L-NAME vehicle subgroup. Our results therefore indicate that normal NO production is essential for the enhanced vascular remodeling induced by exogenous bFGF or VEGF(121) in this rat model of experimental peripheral arterial insufficiency. These results implythat a blunted endothelial NO production could temper vascular remodeling in response to these angiogenic growth factors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 12:33:24