Department of Biomedical Engineering and Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Basic Clin Pharmacol Toxicol. 2012 Jan;110(1):35-41. doi: 10.1111/j.1742-7843.2011.00794.x. Epub 2011 Oct 21.
Blood vessel structure and calibre are not static. Rather, vessels remodel continuously in response to their biomechanical environment. Vascular calibre is dictated by the amount, composition and organization of the elastic extracellular matrix. In addition, the amount and organization of contractile smooth muscle cell (SMC) also need to be regulated. The SMCs are organized such that maximum contractile force generally occurs at diameters slightly below the diameter at full dilation and physiological pressure. Thus, in a remodelling vessel, not only the matrix but also the SMCs need to undergo structural adaptation. Surprisingly little is known on the adaptation of SMC contractile properties in the vasculature. The purpose of this review is to explore this SMC plasticity in the context of vascular remodelling. While not much work on this has been carried out on blood vessels, SMC plasticity is more extensively studied on other hollow structures such as airway and bladder. We therefore include studies on bladder and airway SMCs because of their possible relevance for vascular SMC behaviour. Here, plasticity is thought to form an adaptation allowing maintained function despite large volume changes. In blood vessels, the general match of active and passive diameter-tension relations suggests that SMC plasticity is part of normal vascular physiological adaptation. Vascular SMCs display similar processes and forms of adaptation as seen in nonvascular SMCs. This may become particularly relevant under strong vasoconstriction, when inward cytoskeletal adaptation possibly prevents immediate full dilation. This may contribute to structural inward remodelling as seen in hypertension and flow reduction.
血管结构和口径并非一成不变。相反,血管会不断重塑以适应其生物力学环境。血管口径由弹性细胞外基质的数量、组成和组织决定。此外,还需要调节收缩平滑肌细胞(SMC)的数量和组织。SMC 的组织方式使得最大收缩力通常出现在完全扩张和生理压力下的直径略小的位置。因此,在重塑的血管中,不仅基质,而且 SMC 都需要进行结构适应。令人惊讶的是,关于血管重塑过程中 SMC 收缩特性的适应知之甚少。本综述的目的是探讨血管重塑背景下的 SMC 可塑性。虽然在血管方面这方面的工作很少,但在气道和膀胱等其他中空结构中对 SMC 可塑性的研究更为广泛。因此,我们纳入了膀胱和气道 SMC 的研究,因为它们可能与血管 SMC 行为有关。在这里,可塑性被认为是一种适应机制,即使在体积发生较大变化时也能维持功能。在血管中,主动和被动直径张力关系的一般匹配表明 SMC 可塑性是正常血管生理适应的一部分。血管 SMC 表现出与非血管 SMC 相似的适应过程和形式。在强烈的血管收缩下,这种情况可能尤其重要,此时细胞内骨架的向内适应可能防止完全扩张。这可能导致高血压和血流减少时观察到的结构内向重塑。