Background. In hypertensive patients with angina pectoris, the coronary vasodilator reserve is frequently impaired despite a normal coronary angiogram. Experimental data indicate that structural alterations of the intramyocardial coronary vasculature contribute to an increased minimal coronary resistance and a diminished coronary flow reserve. Methods and Results. In 14 patients (10 men and 4 women) with arterial hypertension and 8 normotensive subjects, minimal coronary resistance and vasodilator reserve (dipyridamole: 0.5 mg/kg body wt, gas chromatographic argon method) were determined after the angiographic exclusion of relevant coronary artery disease. Coronary reserve was depressed in hypertensive patients (2.7+/-2.3 vs 4.6+/-1.3,P less-than-or-equal-to .05) due to increased minimal coronary resistance (0.64+/-0.30 vs 0.24+/-0.05 mm Hg.min.100 g.mL-1, p less-than-or-equal-to 0.002). In right septal biopsies, mean external arteriolar diameter (21.6+/-2.3 vs 17.2+/-2.5 mum, P less-than-or-equal-to .001), mean arteriolar wall area (271+/-61 vs 172+/-62 mum2, P less-than-or-equal-to .01), percent medial wall area (69.9+/-4.0 vs 66.0+/-3.2% W, P less-than-or-equal-to .05), mean periarteriolar fibrosis area (216+/-122 vs 104+/-68 mum2, P less-than-or-equal-to .05), and volume density of total interstitial fibrosis (3.6+/-1.8 vs 1.9+/-0.5Vv% fibrosis, P less-than-or-equal-to .05) were increased in hypertensive patients compared with normotensive subjects. Minimal coronary resistance correlated with %W (r=.6, P less-than-or-equal-to .003) and Vv% fibrosis (r=.62, P less-than-or-equal-to .002). Left ventricular mass index (111+/-21 vs 97+/-17 g/m2, P=NS) and left ventricular end-diastolic pressure (12+/-6 vs 8+/-3 mm Hg, P=NS) did not correlate significantly with minimal coronary resistance. In multivariate analysis, both %W and Vv% fibrosis explained half of the variability of minimal coronary resistance (r2=.5, P less-than-or-equal-to .002). Conclusions. Structural remodeling of the intramyocardial coronary arterioles and the accumulation of fibrillar collagen are decisive factors for a reduced coronary dilatory capacity in patients with arterial hypertension and angina pectoris in the absence of relevant coronary artery stenoses.