SUMMARY 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,
IT is now well established that increased media thickness is associated with hypertension.1 In the spontaneously hypertensive rat (SHR), which is the most studied hypertensive model so far, the cellular basis for the observed medial hypertrophy seems to differ in various vascular beds.2 In the aorta 3 -4 and the superior mesenteric artery, 5 the increased media thickness is associated with hypertrophy, whereas the changes in smaller vessels are probably due to hyperplasia.
-5 - 6 The changes in the conducting arteries are not seen prior to the elevation of the blood pressure, 7 and antihypertensive treatment 8 prevents the structural modifications of the vessels, suggesting that these changes are secondary to hypertension. In contrast, structural alterations in the small muscular arteries and arterioles are present at the prehypertensive and developing hypertensive phases, 7 and these changes