Ischemia-induced angiogenic response is reduced in spontaneously hypertensive rats (SHR). This study determines if exogenous bFGF infusion is effective in expanding collateral circulation in frankly hypertensive SHR. Bilateral femoral arteries of male SHR (weighing ~250 g) were kept intact (Non-occluded control n=9), acutely occluded for 4 hr (n=12), or chronically occluded for 16 d (n=58). Rats in Chronically occluded group were given either vehicle (n=14), or bFGF (0.5 (n=17), 5.0 (n=13) and 50.0 (n=14) µg/kg/d for 14 d) via intra-arterial infusion. Maximal collateral dependent blood flows (BF) to the hind limbs were determined with ⁸⁵Sr and ¹⁴¹Ce labeled microspheres during treadmill running at 20 and 25 m/min at a 15% grade. Pre-exercise heart rates were similar across groups (~530 b/min). Pre-exercise blood pressures (BP) were similar across treatment groups (~200 mmHg across), except in bFGF high dose group where BP was reduced by ~12% (p<0.05). Exercise increased HR and reduced BP (p<0.001). Occlusion of femoral artery for 4 hr resulted in ~95% reduction of BF in the calf muscles during exercise (199±18.7 of Non-occluded group to 10±1.0 ml/min/100 g; p<0.001). BF to the calf muscles of the Vehicle and low-dose bFGF (0.5 µg/kg/d) groups increased over two weeks to 36±3.2 and 45±2.0 ml/min/100 g respectively (p<0.001). bFGF infusion at 5.0 and 50.0 µg/kg/d further increased (p<0.001) BF to the calf muscles (62±4.6 and 62±2.2 ml/min/100 g respectively). Our results show that bFGF can effectively increase collateral dependent BF in hypertensive rats. The reduced hypertension at the high dose of bFGF suggests that a critical signal in arteriogenesis (NO bio-availability) may be restored. These findings suggest that the dulled endothelial NOS of SHR rats does not preempt collateral vessel remodeling.