Adaptation and decompensation of intrarenal small arteries in experimental hypertension.
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.
D000222:Adaptation, Physiological; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000473:pathology*; D001160:Arterioles / Q000473:pathology* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D006977:Hypertension, Renal / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012077:Renal Artery / Q000473:pathology* / Q000503:physiopathology
D000804:Angiotensin II