Acute exposure to high pulse pressure impaired endothelium-dependent dilation in cerebral arteries from young mice, but not old mice, potentially due to greater stiffness in older arteries.
Does ex vivo exposure to high pulse pressure impair endothelium-dependent dilation in isolated cerebral arteries from young and old mice?
Acute exposure to high pulse pressure impairs endothelium-dependent dilation in young, but not old, cerebral arteries, potentially due to the protective effects of age-related arterial stiffness against distension.
One of the hallmarks of vascular aging is increased pulse pressure. This elevated pulse pressure is associated with deleterious effects on cerebral vascular function; however, it is unknown if age modulates the susceptibility to high pulse pressure. To examine the effects of age on the cerebral artery response to pulse pressure, we studied isolated cerebral arteries collected from young (6.1 ± 0.2 mo) and old (26.7 ± 0.5 mo) male C57BL/6 mice. Isolated cerebral arteries were exposed ex vivo to static pressure, low pulse pressure (25 mmHg), and high pulse pressure (50 mmHg). In cerebral arteries from young mice, endothelium-dependent dilation was similar between the static and low pulse pressure conditions. Exposure to high pulse pressure impaired endothelium-dependent dilation in cerebral arteries from young mice, mediated by less nitric oxide bioavailability and greater oxidative stress. Cerebral arteries from old mice had impaired cerebral artery endothelium-dependent dilation at static pressure compared with young cerebral arteries. However, exposure to low or high pulse pressure did not cause any further impairments to endothelium-dependent dilation in old cerebral arteries compared with static pressure. The old cerebral arteries had less distension during exposure to high pulse pressure and greater stiffness compared with young cerebral arteries. These results indicate that acute exposure to high pulse pressure impairs endothelium-dependent dilation in young, but not old, cerebral arteries. The greater stiffness of cerebral arteries from old mice potentially protects against the negative consequences of high pulse pressure.
Winder et al. (Fri,) conducted a other in Vascular aging and cerebral artery endothelial function. High pulse pressure vs. Static pressure and low pulse pressure (25 mmHg) was evaluated on Endothelium-dependent dilation. Acute exposure to high pulse pressure impaired endothelium-dependent dilation in cerebral arteries from young mice, but not old mice, potentially due to greater stiffness in older arteries.