Vascular lesions are the major cause of morbidity and mortality in hypertensive patients. However, the pathologic characteristics of gradually evolving, chronic hypertension have not been adequately studied and the mechanism by which hypertension accelerates atherosclerosis is still uncertain. This study was undertaken to invertigate the ultrastructural changes of the aorta and the effect of high cholesterol diet in spontaneously hypertensive rats(SHR).

Spontaneously hypertensive rats (n=80, male, 5 weeks old) and Wistar rats (n=40, male, 5 week old) were used. Forty SHR were fed with 2% cholestrol diete, while the remainder with control diet. Systolic blood pressure was measured weekly until 16 weeks after birth, and then biweekly until 40 weeks after birth. Transmission and scanning electron microscopy were used to evaluate ultrastrucural changes of the aorta.

1) The blood pressure of SHR rose stedily and progressively from the 5 weeks after birth and reached nearly 190mmHG at the 16 weeks after birth. 2) In SHR, the subendothelial component contained finely granular substances, abundant fibrillar collagen and elastin. Infiltration of the mononuclear blood leukocytes into the intima was frequently seen. 3) Endothelium from cholestrol-fed SHR did exhibit numerous pinocytotic vesicles and contained many cytoplasmic filaments. There were a number of large mononuclear lipid-filled cells in the intimal lesions. Blistering of the endothelial plasma membrane was also observed in high cholesterol diet-fed SHR. Later on, adhesion of platelets, febrin, and white blood cells as well as damage of intima shown as multiple small holes were more marked. 4) There was no significant difference in systoloic blood pressure between high cholesterol diet-fed and control diet-fed SHR.

In the aorta of SHR, the most prominent change was an expansion of the subendothelial space and infiltration of the mononuclear leukocytes into the intima. The present study showed that the SHR was indeed a reliable model for the essential hypertension. In some SHR, high cholesterol diet could induce more pronounced vascular lesions, which were enhanced by hypertension.