Action of cholestane-3 beta,5 alpha,6 beta-triol on rats with particular reference to the aorta

Cholestane-3 beta,5 alpha,6 beta-triol, administered orally to rats in different doses and for varying lengths of times, effected toxic cell damage on aortic smooth muscle cells and endothelium. Cholesterol, applied in the same doses, did not lead to appreciable alterations of the aorta. After parenteral application of lipids with simultaneous administration of cholestane-triol there were no demonstrable fat deposits in the damaged aortic wall with angiotensin II (AII) induced hypertension. Thus, there was no recognizable influence of hypertension on increased fat passage in the arterial wall, or any action of lipids to enhance the permeability of vessels. However, the hypertension had an exacerbating effect in so far as in animals with AII-induced blood pressure rise alterations of the media were more pronounced after cholestane-triol, although we were unable to rule out a primary effect of AII. A potentiation of the cholestane-triol action by simultaneous application of cholesterol demonstrated for the rabbit did not occur in rats. Blood content was lowered mostly by cholestane-triol, also by cholesterol. HDL-cholesterol was little affected; almost no influence was observed in triglycerides. The strong cytotoxic action of cholestane-triol underlines its health-damaging role. Due to its action on the aorta of the rat, despite the animal's resistance to arteriosclerosis, involvement of this cholesterol derivative in the pathogenesis of arteriosclerotic alterations can not be excluded.