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Increased vascular resistance in spontaneous hypertension has been attributed to a reduced arteriolar lumen and a decrease in the number of arterioles and capillaries. In the present study, microvascular mechanisms for increased resistance were investigated in the cremaster muscle of 5-6-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY) using intravital microscopy. Vessels were classified on the basis of their location in the network relative to their branching order and function (A1—A4). In each preparation, one vessel of each category was observed for its side-branches, using bright-field microscopy. By comparing the number of side-branches seen under control conditions and after maximal vasodilatation (10~3mol/l adenosine, topically) we assessed their functional reserve. Capillary density was investigated using incident fluorescence microscopy. Both under control conditions and after vasodilatation, mean arterial pressure and heart rate were increased in SHR (mean arterial pressure: SHR 103±4mmHg, WKY 89 ± 3mmHg, P<0.05; heart rate: SHR 380 ± 16 beats/min, WKY 343 ± 12 beats/min, P<0.05). Arterioles (A1-A4) of SHR and WKY were equal in diameter (SHR: 75.8 ± 3.2, 48.7 ± 1.1, 21.4 ± 0.9, 10.0 ± 0.04 ^m; WKY: 71.6 ± 2.4, 48.9 ± 1.1, 18.5 ± 0.9, 9.8 ± 0.3 urn; A1-A4, respectively). After adenosine, the relative increase in diameter was similar in both groups. The number of side-branches under control conditions was similar in A1 and A2 vessels. SHR had fewer A3 vessels per A2 and fewer A4 vessels per A3 (per unit length), indicating a diminished arteriolar reserve. SHR capillary density was lower under control conditions (SHR 33.1 ± 1.2 mm/mm2; WKY 44.9 ± 1.7 mm/mm2; P<0.05). No capillary recruitment occurred during adenosine administration. We conclude that, in the early phase of spontaneous hypertension, a structurally diminished functional arteriolar reserve and a reduced capillary density, rather than a decreased dilating capacity or a reduced vessel lumen, are the primary mechanisms leading to the increased vascular resistance in cremaster muscle.