Focal patterns of <sup>3</sup>H-cholesterol uptake were demonstrated in the macroscopically normal 'lesion free' young pig aorta with the aid of the protein-binding azo dye Evans blue. The transmural distribution of labelled cholesterol in areas of both high and low aortic <sup>3</sup>H-cholesterol uptake were studied at intervals from 10 min. to 24 hr. after the intravenous injection of 1.5 mCi of <sup>3</sup>H-cholesterol. Cholesterol gradients were determined using serial 100 μ frozen sections from the endothelial surface to the adventitia, and the results expressed as the dpm 100 mg. dry weight, or dpm mg. DNA. <sup>3</sup>H-Cholesterol entered the aorta rapidly and by 10 min. there was an appreciable distribution throughout the intima, media and adventitia. By 24 hr. most cholesterol activity was concentrated in the intima and inner media. In areas of both high and low cholesterol uptake, cholesterol activity in the media increased with time after the injection of label. In areas of high cholesterol uptake, identified by the intimal accumulation of Evans blue, the <sup>3</sup>H-cholesterol activity within the intimal 200 μ was greater than in areas of low uptake. At 24 hr., the label was predominantly associated with unesterilied cholesterol, which showed a distribution gradient similar to that of total cholesterol. Esterified cholesterol activity was minimal, and distributed evenly throughout thc aortic wall. Both free cholesterol activity and free cholesterol specific activity were greater in blue than in white areas, and these differences persisted through most of the aortic wall. Free cholesterol and DNA content and distribution across the vessel wall were similar in blue and white areas. The results suggested that the increased uprake of labelled cholesterol by blue areas reflects a higher free cholesterol turnover in these areas, and that the intima is the principal point of entry of the labelled plasma cholesterol <i>in vivo</i>. This model can be used in the study of the very early structural and metabolic changes in atherogenesis.