The effect of changes in pulse pressure on artery structure and function
Pulse Pressure (PP), the difference between systolic and diastolic pressure, is a defining characteristic of the blood flow in the body, which alters due to cardiovascular diseases and their treatments. The purpose of this project was to examine the effect of an increase or decrease in pulse pressure on the artery function, cellular function, and extracellular matrix remodeling. Porcine common carotid arteries were cultured under non-pulsatile pressure (100 mmHg), pulsatile pressure (70-130 mmHg), or hyper-pulsatile pressure (50-150 mmHg) for 24 hours, 3 days, or 7 days in an ex vivo organ culture model. Vasomotor response, wall permeability, cell proliferation, and apoptosis were examined after three and seven days. MMP-2, MMP-9, caveolin-1, and a-actin levels were examined using immunoblotting, while collagen and elastin were examined using immunohistochemistry after three and seven days. VCAM-1, ICAM-1, MCP-1, VE-cadherin and occludin were all examined using quantitative RT-PCR after 24 hours and three days. Our results showed that hyper-pulsatile pressure decreased the artery response to SNP and wall permeability. Non-pulsatile pressure caused an increase in cell proliferation. Neither hyper-pulsatile pressure nor non-pulsatile pressure caused a change in the ECM or in the expression of MMP-2, MMP-9, caveolin-1, or alpha-actin. Hyper-pulsatile pressure increases MCP-1 gene expression; however, the increase was not accompanied by changes in ICAM-1 or VCAM-1. No other changes in gene expression were detected. Taken together, these changes indicate that pulse pressure has a limited effect on the artery immediately after its application. Specifically an increase in pulse pressure alters the artery tone and wall permeability while a decrease in pulse pressure alters cell proliferation. These results improve our understanding of how a change in pulse pressure affects the artery and its function.