To determine whether the increased thickness seen in media of mesenteric resistance vessels of Wistar-Kyoto rats made hypertensive by a Goldblatt procedure (one-kidney, one clip model) was due to hypertrophy or hyperplasia of smooth musde cells, the cellular dimensions of these vessels were estimated using a new, unbiased stereoJogkal method (the disector). Furthermore, to investigate whether the changes seen could be secondary to the increased blood pressure, morphometric measurements were also made in renal arcuate arteries, which, due to the constricting silver clip, probably had not been exposed to the increased pressure load. Vessels were mounted on a myograph, and their media thickness, lumen diameter, and maximum active wall tension response were measured. In the mesenteric vessels media thickness had increased by 58%, whereas no changes were seen In the renal vessels. Vessels were then fixed, and serial sections were made in the mesenteric vessels. The disector was used to calculate the numerical cell density in each vessel. By combining the myograph measurements and the estimated numerical cell density, the number of cells per segment unit length was calculated (renal hypertensive rats, 6.8 μm−1; sham-operated Wistar-Kyoto rats, 6.3 μm−1;Pgt; 0.40) and mean cell volume was determined (renal hypertensive rats, 1541 μm3; sham-operated Wistar-Kyoto rats, 1256 μm3;p< 0.02). No morphometrkal changes were found hi single sections of the renal arteries. We conclude that the Increased media thickness observed in mesenteric resistance vessels of one-kidney, one dip Goldblatt hypertensive rats mainly was caused by smooth muscle cell hypertrophy.