This study evaluated the possibility that hi hypertension, mechanisms that maintain near normal arteriolar diameters at elevated arteriolar pressures limit the ability of skeletal muscle arterioles to dilate hi response to an increase hi tissue metabolism. The spinotrapezius muscles of 16- to 20-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were contracted at frequencies of 1, 2, 4, and 8 Hz. The inner diameters of first-order through third-order arterioles were measured at rest and following 3 minutes of contractions. Tissue oxygen tension (PO2) at the venous end of capillaries was monitored during 8-Hz contractions. At rest, following contractions, and after nurrimnm dilation with adenosine, the inner diameters of arterioles of equivalent branch order were not significantly different hi SHR and WKY. Opening of closed arterioles during musde contraction and adenosine application occurred hi less than 5% of the observations hi both groups. The resting tissue Po2was 25.5 ± 1.3 mm Hg hi normal rats and 26.1 ± 2.1 mm Hg hi SHR. At nearly maximum vasodilation during 8-Hz stimulation, tissue PO2] recovered to 81.9 ± 12.7% of control In WKY but only to 41.2 ± 13.0% of control hi SHR. These observations indicate that the expression of local regulatory mechanisms related to tissue metabolism is virtually normal In the spinotrapezius muscle vasculature of SHR in the context of arteriolar dilation. However, at near maTinwni performance, factors other than absolute arteriolar diameter preclude the normal preservation of tissue PO2in the spinotrapezius musde of SHR.