Humphrey Jay D, Wilson Emily
Department of Biomedical Engineering and M.E. DeBakey Institute, Texas A&M University, 233 Zachry Engineering Center, College Station, TX 77843-3120, USA.
J Biomech. 2003 Nov;36(11):1595-601. doi: 10.1016/s0021-9290(03)00178-7.
A conspicuous long-term consequence of hypertension is a thickening of the arterial wall, which many suggest returns the circumferential wall stress toward its normal value. This thickening results from an increase in smooth muscle and extracellular matrix, with the associated growth and remodeling processes depending on a host of regulatory signals that likely include the altered mechanical environment. Although the precise mechanotransduction pathways remain unknown, we propose that vasoconstriction may be an early response of the arterial wall to a step-change in pressure. In particular, computations suggest that such a response can decrease the magnitude and transmural gradients of the pressure-induced wall stresses and return the mean wall shear stress toward its homeostatic value. Such an initial 'compensatory vasoconstriction' could also help set into motion subsequent growth and remodeling responses due to growth regulatory characteristics of the vasoactive molecules (e.g., nitric oxide, endothelin-1, angiotensin-II). Although the consequences of growth and remodeling have been the focus of prior biomechanical and histological studies, early responses dictate subsequent developments and therefore deserve increased attention in vascular biomechanics and mechanobiology.
高血压一个显著的长期后果是动脉壁增厚,许多人认为这会使周向壁应力恢复到正常水平。这种增厚是由平滑肌和细胞外基质增加导致的,相关的生长和重塑过程取决于许多调节信号,这些信号可能包括改变的力学环境。尽管精确的机械转导途径仍然未知,但我们认为血管收缩可能是动脉壁对压力阶跃变化的早期反应。具体而言,计算表明这种反应可以降低压力诱导的壁应力的大小和跨壁梯度,并使平均壁剪切应力恢复到其稳态值。这种初始的“代偿性血管收缩”也可能由于血管活性分子(如一氧化氮、内皮素-1、血管紧张素-II)的生长调节特性而有助于启动后续的生长和重塑反应。尽管生长和重塑的后果一直是先前生物力学和组织学研究的重点,但早期反应决定了后续发展,因此在血管生物力学和力学生物学中值得更多关注。