Transendothelial lipid transport into and spread in the subendothelial intima of large arteries, and subsequent lipid accumulation appear to start plaque formation. We experimentally examine transendothelial horseradish peroxidase (HRP) transport in vessels that are usually, e.g., pulmonary artery (PA), or almost always, e.g., inferior vena cava (IVC), atherosclerosis resistant vs disease-prone, e.g., aorta, vessels. In these vessels, HRP traverses the endothelium at isolated, focal spots, rather than uniformly, for short circulation times. For femoral vein HRP introduc-tion, PA spots have 30s radii~ (53.2µm SD10.4) (compare aorta: 54.6µm SD8.75), grow quickly from 30s-1min (40%, P<0.05) and more slowly afterwards (P>0.05). This trend resembles the aorta, suggesting the PA has a similarly sparse intima. With carotid artery HRP introduction, the 30s spot (132.86±37.32 µm) is far larger than the PA's, grows little (~28%, P<0.05) from 30-60s and is much flatter than the artery curves. Transverse EM sections after ~10 min HRP circulation show thin, intense staining immediately beneath both vessels' endothelia with an almost step change to diffuse staining beyond. This indicates the existence of a sparse, subendothelial intima, even when there is no internal elastic lamina (IVC). This motivates a simple model that translates growth rates into lower bounds for the flow through focal leaks. The model results and our ear-lier wall and medial hydraulic conductivity data explain these spot growth curves and point to differences in transport patterns that might be relevant in understanding the IVC's immunity to disease initiation.