Previous physiological studies have suggested that loss of microvessels (anatomic rarefaction) occurs in the skeletal muscle microcirculation of rats with chronic hypertension. However, little is known of the exact structural changes that occur during the process of anatomic rarefaction. The purpose of this study was to examine the muscle at the ultrastructural level to search for evidence of microvessel degeneration that would correlate with the concept of anatomic rarefaction in chronic hypertension. Cremaster muscles were removed from normal rats and from rats with chronic reduced renal mass hypertension, which was produced by a 75% reduction in kidney mass followed by salt loading (4% NaCl chow with water ad libitum) for 4 weeks. The muscles were fixed and prepared for histological examination by light and electron microscopy. Atrophy and degeneration of both endothelial cells and vascular smooth muscle cells were observed in many arterioles of the hypertensive rats. Some arterioles of hypertensive rats were degenerated to such an extent that the original identity of the cells could not be determined. The hypertensive rats also exhibited degeneration of capillaries and extravasation and uptake of red blood cells into lymphatic vessels. In contrast, age-matched control rats exhibited normal histology. The results of this study support previous physiological evidence for anatomic rarefaction in the cremaster muscle of chronically hypertensive rats.