The role of mechanical and humoral factors in growth regulation of vascular smooth muscle and cardiac myocytes.
The role of mechanical and humoral factors in growth regulation of vascular smooth muscle and cardiac myocytes.
复制标题
机械和体液因素在血管平滑肌和心肌细胞生长调节中的作用。
DOI：
10.1097/00041552-199301000-00004
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发表时间：
1993
影响因子：
3.2
通讯作者：
Dzau,VJ
中科院分区：
文献类型：
--
作者：
Dzau,VJ
心脏和血管的结构变化参与心血管系统的长期调节。在高血压和心肌功能障碍中，心脏和血管重构的适应性过程可能有助于这些疾病的病理生理和并发症。最近的研究提高了我们对血管平滑肌和心肌细胞生长的细胞和分子生物学的理解。机械和神经激素因素可以独立地刺激血管和心肌细胞的肥大增生。心肌细胞和血管平滑肌细胞的压力-牵张增加可激活原癌基因表达，从而介导生长反应。血管活性物质也调节心血管生长。一般而言，内源性血管收缩剂（如血管紧张素、内皮素）可作为血管平滑肌生长促进剂，内源性血管扩张剂（如一氧化氮、前列环素、心房利钠肽）可作为血管平滑肌生长抑制剂，可能还包括心肌细胞。最近的数据表明，血管收缩剂，如血管紧张素，激活原癌基因和自分泌生长因子，介导血管生长。此外，血管肥大与增生的发生取决于生长刺激物对内源性增殖生长因子（例如血小板衍生生长因子、碱性成纤维细胞生长因子）与抗增殖因子（例如转化生长因子-[β]）的相对激活。总之，这些数据表明，复杂的相互作用的局部介质，参与心血管疾病的病理生理学，控制心血管生长。
Structural changes of the heart and blood vessels participate in the long-term regulation of the cardiovascular system. In hypertension and myocardial dysfunction, the adaptive process of cardiac and vascular remodeling may contribute to the pathophysiology and complications of these diseases. Recent investigations have enhanced our understanding of the cellular and molecular biology of vascular smooth muscle and cardiac myocyte growth. Mechanical and neurohormonal factors can independently stimulate hypertrophy-hyperplasia in vascular and cardiac myocytes. Increased pressure-stretch of cardiac myocyte and vascular smooth muscle cells can activate protooncogene expressions that may mediate the growth response. Vasoactive substances also regulate cardiovascular growth. In general, endogenous vasoconstrictors (eg, angiotensin, endothelin) act as growth promoters, and endogenous vasodilators (eg, nitric oxide, prostacyclin, atrial natriuretic peptide) act as growth inhibitors of vascular smooth muscle and, possibly, cardiac myocytes. Recent data have demonstrated that the vasoconstrictive agents, such as angiotensin, activate protooncogenes and autocrine growth factors that mediate vascular growth. Furthermore, the development of vascular hypertrophy versus hyperplasia is dependent on the relative activation of endogenous proliferative growth factor (eg, platelet-derived growth factor, basic fibroblast growth factor) versus antipro-liferative factor (eg, transforming growth factor-[beta]) by the growth stimulus. Taken together, these data demonstrate that complex interactions of local mediators, which participate in the pathophysiology of cardiovascular diseases, control cardiovascular growth.