[Morphogenesis of central and peripheral arteriopathies in the spontanously hypertensive rat. 1. Histological characteristics]

Numerous elastic and muscular arteries and arterioles of the SHR and Wistar Kyoto were morphologically and comparatively studied before (4th week) and after (20th, 30th and 60th week) high blood pressure set in. The vascular changes observed occurred after the increase in blood pressure, were proportional to its duration, and differed in frequency and intensity: myocyte hypertrophy, medial thickening and fibrosis (omnipresent) greater than cell proliferation and migration, lymphomonocyte invasion, intima thickening (localised) greater than signs of degeneration (vacuolar, hyaline); necrosis and repair (late - 60th week and scattered). The morphogenesis of SHR arteriopathy was characterised by the pre-eminence of cell phenomena over insudation phenomena. Three processes of unequal importance (myocyte hypertrophy, connective neogenesis greater than myocyte hyperplasia) lead to a thickening of the arterial and arteriolar media (vascular wall adaptation to the increased blood pressure). The intimal fibro-muscular thickening (scattered and unevenly distributed) arose from reactions of local arterial cells (migration and proliferation) and lymphomonocyte immigration. The chronology and severity of lesions presented certain variations from some arteries to others i.e. more pronounced reaction of the media in the central vasculature; those in the intima were more extensive and serious at orifices and bifurcations and in small arteries and arterioles (obstructive arteriolopathy); heart and kidney vasculatures were affected earlier and more seriously. The "atherogenic impact" of the medial fibrosis and thickening, of obstructive arteriolopathy in vasa vasorum, of the increase in glucosaminoglycan content, and of the invasion by platelets and monocytes was discussed.