In the presence of
hypertension, the arterial and arteriolar vessel walls may undergo adaptive, destructive, and reparative changes. These different types of hypertensive alterations were studied simultaneously in the intrarenal vascular bed of two-kidney, one-
clip hypertensive rats. After constriction of one renal artery, focal medial
necrosis of the interlobular arteries developed in the untouched kidneys after the first 24 h. These earliest signs of vascular decompensation could be explained by short-lasting hypertensive episodes that were only detectable by continuous blood pressure recording in conscious animals. Two weeks after the experiment was started, owing to a widening of the media, a substantial increase in the wall-to-lumen ratio was observed in the interlobular arteries. At the same time, the frequency of focal medial
necrosis began to fall significantly. Therefore we concluded that the structural vascular adaptation might be responsible for the disappearance of focal medial
necrosis in spite of still rising blood pressure values. This assumption was confirmed by an additional experiment in previously chronically two-kidney, one-
clip hypertensive rats: 24 h after removing the renal artery
clip, a short, severely hypertensive period, induced by infusions of
angiotensin II, caused hypertensive vascular lesions almost exclusively in the primarily clipped kidneys with a nonadapted vascular bed. Early intimal changes, which are known to lead to malignant
nephrosclerosis, were not only absent in the beginning of two-kidney, one-
clip hypertension, but also did not occur during the
angiotensin-induced accelerated
hypertension. Thus, even extremely
high blood-pressure values per se may not be enough to initiate this crucial renal
vascular disease.