To examine the influence of hydrostatic pressure on low density lipoprotein (LDL) flux in the artery wall, LDL was fluorescently labeled and perfused into rat carotid arteries. The rate of LDL accumulation was measured by quantitative fluorescence microscopy. At hydrostatic pressures of 60. 90, 120 cm H2O, the rates of LDL accumulation were 0.17 0.06, 0.4 0.12 and 0 78 0.25 mV/min, respectively (n=6 arteries). Significant difference in the rates of LDL accumulation were observed at 60 and 120 cm H2O (p = 0.03). The regression coefficient of the rate of LDL accumulation on hydrostatic pressure was 0.3 (r2=0.97). We compared the rate of accumulation of a similar-sized, nonlipid molecule (2,000,000 MW dextran). The rates of dextran accumulation in 6 perfused arteries were 0.11 0.07, 0.13 0.03 and 02 0.05 mV/min at hydrostatic pressures of 60, 90, 120 cm H2O, respectively. No significant differences in the rates of dextran accumulation were noted at any hydrostatic pressure. The regression coefficient of the rate of dextran accumulation on hydrostatic pressure was 0.065 (r2=0.96). Thus, increased hydrostatic pressure selectively increases the rate of LDL accumulation more than dextran accumulation (p<0.002). Our studies suggest binding or entrapment of LDL within the artery wall. In hypertensive patients this observation may be important in atherogenesis.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology