Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced α-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia. To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine. Fractional flow reserve(FFR, calculated by coronary pressure measurements during adeno sine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis(mean diameter stenosis of 50±1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an α1-, α2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective α1-adrenergic blocker;(c) 20 patients before and after IC bolus of saline. Since minimal luminal diameter remained unchanged before and after phentolamine(1.46±0.06 vs. 1.47±0.06 mm, ns), urapidil 1.46±0.06 vs. 1.39±0.08, ns), and saline(1.56±0.08 vs. 1.55±0.08, ns), changes in FFR reflects changes in microvascular resistance. Overall, phentolamine and urapidil induced a slight but significant decrease in FFR(phentolamine: 0.79±0.02 vs. 0.77±0.02, p< 0.05; urapidil: 0.78±0.02 vs. 0.75±0.02, p< 0.05). However, only 6 patients showed a change in FFR from ≥0.75 to < 0.75 and no patients showed a change in FFR from ≥0.80 to < 0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure. The administration of α-adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values do not significantly affect clinical decision making. Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced α-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia. To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine. Fractional flow reserve (FFR, calculated by coronary pressure measurements during adeno sine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis (mean diameter stenosis of 50 ± 1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an α1-, α2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective α1-adrenergic blocker; (c) Since minimal luminal diameter filed unchanged before and after phentolamine (1.46 ± 0.06 vs. 1.47 ± 0.06 mm, ns), u rapidil 1.46 ± 0.06 vs. 1.39 ± 0.08, ns), and saline (1.56 ± 0.08 vs. 1.55 ± 0.08, ns), changes in FFR reflects changes in microvascular resistance. Overall, phentolamine and urapidil induced a slight but significant decrease in FFR (phentolamine: 0.79 ± 0.02 vs. 0.77 ± 0.02, p <0.05; urapidil: 0.78 ± 0.02 vs. 0.75 ± 0.02, p <0.05) However, only 6 patients showed a change in FFR from ≥ 0.75 to <0.75 and no patients showed a change in FFR from ≥0.80 to <0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure. The administration of α -adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values ​​do not significantly affect clinical decision making.