[Hypertensive arteriopathy: aortic histo-metabolic changes during postnatal ontogenesis in spontaneous hypertensive rats (Okamoto-Aoki strain) (author's transl)].

27 aortic histoenzymatic activities and 6 aortic macromolecular substances were comparatively studied in spontaneous hypertensive rats (SHR) and normotensive Wistar rats (3, 5, 13 and 16 month-old). The earlier aortic changes (3rd month) were only histoenzymatic: 5 Nase and LDH were increased in the entire aorta: some oxido-reductases increase near the intima. These early minor changes might represent some of the factors of the functional disturbance of the arterial smooth muscle cell. At the stage of stable hypertension (5th-13th month) two lesion patterns were seen: 1) metabolic: increase of the histoenzymatic activities involved in lipolysis, GAG anabolism, glycolysis, cell respiration, energizing metabolism and nucleotides-esterolysis. 2) Structural: cell hypertrophy and hyperplasia, interstitial fibrosis. The stimulus of the metabolic changes seems to be dual: 1) the hypertensive factor acting upon smooth muscle cells and/or vasa vasorum. 2) The intraarterial pressure increasing endothelial crossing and stimulating myocyte contraction. The structural change is more probably the reaction to elevated pressure; it has led to diffuse medial thickening providing a balance between hypertension and arterial wall stress. On the 16th month, the cell reaction developed in two ways: 1) increase of metabolic and morphogenetic activation of some cells. 2) irreversible degeneration in some other cell groups (media necrosis, cicatricial fibrosis, decrease of oxidoreductases and lipolytic activities, increase of lysosomal enzymes). Aortic lesions during spontaneous hypertension were less dramatic and occurred later than after experimental hypertension. Some of the observed histometabolic changes might lead to maintenance and worsening of hypertension.