Pathogenesis of acute arterial fat deposition in spontaneously hypertensive rats.
The selectively-bred substrains of spontaneously hypertensive rats with a greater vulnerability to vascular lesions rapidly developed arterial fat deposition within 1 or 2 weeks as well as a greater hypercholesterolemic response when fed on high fat cholesterol diet including 20% of suet, 5% of cholesterol and 2% of cholic acid. The ring-like arterial fat deposition at the branches of superior mesenteric arteries and cerebrobasal arteries, which was found to be good indices for the deposition of intrarenal or coronary arteries, was not observed in normotensive rats fed on high fat cholesterol diet for 3 months, greatly delayed in SHR under antihypertensive treatment and accelerated by 1% salt loading in drinking water. The horseradish peroxidase infused intravenously 1 to 4 hours before sacrifice leaked in ring-like forms which corresponded to the fat deposit in mesenteric arteries. The incorporation of 3H-proline infused 4 hours before sacrifice was enhanced in the mesenteric arteries with the fat deposition. These results clearly indicated that hypertension was a great contributory factor to rapid arterial fat deposition, which was caused by an increased vascular permeability and enhanced the arterial collagen formation, the initiation process of arterio- or atherosclerosis.
D000208:Acute Disease; D000818:Animals; D001158:Arteries / Q000378:metabolism*; D002199:Capillary Permeability; D002536:Cerebral Arteries / Q000378:metabolism; D002791:Cholesterol, Dietary / Q000378:metabolism; D006830:Hydralazine / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D050356:Lipid Metabolism; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism; D051381:Rats
D002791:Cholesterol, Dietary; D006830:Hydralazine