Effects of pressure-induced stretch and convection on low-density lipoprotein and albumin uptake in the rabbit aortic wall.

The effects of pressure-driven convection and vessel wall stretching in the pressure-related changes in low-density lipoprotein (LDL) and albumin transport across the arterial wall were studied in vitro in freshly excised rabbit thoracic aorta held at in vivo length and pressurized at 70, 120, or 160 mm Hg for 30 minutes. External rigid polyester sleeves of various diameters (4, 5, or 6 mm) were passed around half of the arterial segments in order to prevent vessel distension during pressurization. The intraluminal solution contained 131I-LDL and 125I-albumin. The transmural distribution of relative concentrations of LDL (CLDL) and albumin (Calb) across the wall was determined in wrapped and unwrapped segments using a serial frozen-sectioning technique. In the unwrapped segments, Calb increased uniformly between 70 and 120 mm Hg (P < .0001) but did not change significantly between 120 and 160 mm Hg (0.0063 +/- 0.0009 [n = 4], 0.0520 +/- 0.0055 [n = 9], and 0.0620 +/- 0.0071 [n = 12], respectively). In contrast, CLDL increased markedly both between 70 and 120 mm Hg (P < .001) and between 120 and 160 mm Hg (P < .05) (0.0025 +/- 0.0005 [n = 4], 0.0234 +/- 0.0029 [n = 9], and 0.0393 +/- 0.0056 [n = 12], respectively), with the increase being much more pronounced in the inner than in the outer media. In the segments wrapped with the 4-mm sleeves, both CLDL and Calb did not vary significantly between 70, 120, and 160 mm Hg. In the segments wrapped with the 5-mm sleeves, CLDL increased significantly between 120 and 160 mm Hg, whereas Calb did not vary significantly with increasing pressure. Our results demonstrate that (1) pressure-induced stretching of the arterial wall is a major determinant of arterial mass transport, and (2) pressure-driven convection accentuates LDL accumulation in the inner media, which may explain enhanced atherosclerosis in hypertension.