1. The ultrastructural and histochemical analyses of renal small arteries in forty hypertensive patients (ages ranged from 20 to 63 years) and forty normotensive ones (from 18 to 60 years) were performed.
Lysosomes containing lipid droplets and electron-dense structures were demonstrated in the center of smooth muscle cells. Around lysosomes Golgi complexes were well-developed, also numerous mitochondria and ribosomes were accumulated. These lysosomes were noted in all cases studied without regard to the presence or abscence of hypertension.
The basic pattern of the electron-dense structures within lysosomes appeared to be a series of three layers with a total thickness of 60-80Å like a unit membrane. These three-layered structures were parallelly arranged with the fundamental spacing of 40-50Å. The present authors call this pattern “the lamellar structure” within lysosomes. The examination in high magnification revealed that the lamellar structures showed several patterns such as the lamellar phase, the latticed phase, the hexagonal phase and the amorphous phase. These various patterns probably arose from a different orientation of the three-dimentional structure with respect to the direction of view. But there remained many obscure points about the lamellar structure. Further detailed studies will be required.
2. Male SHRSP of 10 weeks, 16 weeks and 20 weeks old were killed by perfusion fixation method with Karnovsky solusion. After the perfusion fixation cerebral arteries were dissected up to the periphery as much far as possible. The present authors observed various morphological changes in the cerebral arteries and analyzed the developmental mechanisms at work in these changes. In the main portion of cerebral arteries, both of endothelial and medial cells were almost always well-preserved. In a smaller number were observed degenerative or necrotic changes of smooth muscle cells especially next to the adventitia. Regressive changes were not found in endothelial cells at all.
Cerebrovascular changes were more prominent in the branches, especially surrounded by 1-2 layers of medial smooth muscle cells. In the cerebral arteries of SHRSP the medial damage appeared to precede the intimal degeneration. The hypertensive medial damages, characterized by degeneration, necrosis and disappearance of smooth muscle cells, were initially observed in cell bodies adjacent to the adventitia. In these lesions the present authors found two types of necrotic changes of smooth muscle cells. The first type was the Focal Cytoplasmic Necrosis (FCN), which fundamentally consisted of dense-granular substances. FCN also contained spindle-like structures, abundant cell debris and degenerated mitochondria. FCN appeared to have a close relation to giant vacuole formation in the cytoplasm.
The second type was characterized by reduction and disarrangement of myofilaments, and disappearance of cristae in mitochondria. These two types of necrotic changes were primarily associated with the disappearance of smooth muscle cells. In contrast endothelial cells were almost intact in the branches which had advanced medial damages. However in the area where the branches completely lost medial smooth muscle cells, various regressive changes, such as degeneration of cell organellae and giant vacuole formation, were noted. It was a point of importance that interendothelial junctions were well-preserved even in endothelial cells with advanced medial damages. Lysosomes were constantly small in size and were scarcely found in medial muscle cells. It was noteworthy that lysosomes did not appear to have a relation to the necrotic change of cell bodies.
