Quantitative structural changes of the rat thoracic aorta in early spontaneous hypertension. Tissue composition, and hypertrophy and hyperplasia of smooth muscle cells.

The thoracic aorta of 21-, 28-, 35-, and 45-day-old spontaneously hypertensive (SH) and Wistar Kyoto (WK) rats was analyzed morphometrically to evaluate the cellular hypertrophy and proliferation of medial smooth muscle cells during the development of genetically determined hypertension. The absolute increase in volume of collagen and ground substance, and elastic tissue was also measured. In SH animals, cellular hypertrophy was found to be the dominant mechanism of muscle growth in the 21- to 28-day and 35- to 45-day intervals, resulting in an overall 68% enlargement of the mean cell volume from 21 to 45 days. The total number of smooth muscle cells increased only 21% (not statistically significant) and the tendency toward hyperplasia was restricted to the 28- to 35-day period. Normotensive controls showed cell proliferation mainly from 21 to 28 days and cellular hypertrophy from 35 to 45 days with an absolute 33% increase in the number of cells and a 26% larger volume of the mean smooth muscle cell at 45 days of age. from 21 to 45 days, the above changes in cell size and number provoked an overall 104% and 67% growth of the muscle mass in SH and WK rats, respectively. The initial response phase of spontaneous hypertension was also characterized by an increase of collagen and ground substance, 184%, which was slightly greater than that of the elastic component, 168%. Changes in mural concentration of fibrous proteins that were similar to but of less magnitude than those of controls, were seen. These results demonstrate that short-term spontaneous hypertension determines a simultaneous growth adaptation in every component structure of the media of the thoracic aorta leading to a disproportionate accumulation of scleroproteins that markedly exceeds that of the contractile component of the vessel wall. At a cellular level, smooth muscle cell hypertrophy is the prevailing process that underlies the tissue response of the aorta in early hypertension.