Touyz R M
Clinical Research Institute of Montreal, 110 Pine Avenue West, Montreal, Quebec H2W 1R7, Canada.
Can J Cardiol. 2000 Sep;16(9):1137-46.
Human essential hypertension is a complex, multifactorial, quantitative trait under polygenic control. The fundamental hemodynamic abnormality in hypertension is increased peripheral resistance due primarily to changes in vascular structure and function. These changes include arterial wall thickening and abnormal vascular tone, and are due to alterations in the biology of the cellular and noncellular components of the arterial wall. Multiple interacting humoral and mechanical factors as well as oxidative stress stimulate complex signalling pathways, which modulate vascular smooth muscle cell contraction and growth. Under normal physiological conditions, these finely regulated processes maintain vessel wall integrity and prevent pathological increases in blood pressure. However, under abnormal conditions, increased humoral and mechanical signalling results in vascular wall thickening and increased vascular tone, which play an important role in the pathogenesis and maintenance of hypertension. The present review discusses recent developments in the understanding of cellular and molecular mechanisms underlying vascular regulation in hypertension.
原发性高血压是一种受多基因控制的复杂、多因素定量性状。高血压的基本血流动力学异常是外周阻力增加,主要是由于血管结构和功能的改变。这些变化包括动脉壁增厚和血管张力异常,是由动脉壁细胞和非细胞成分生物学改变引起的。多种相互作用的体液和机械因素以及氧化应激刺激复杂的信号通路,调节血管平滑肌细胞的收缩和生长。在正常生理条件下,这些精细调节的过程维持血管壁完整性,防止血压病理性升高。然而,在异常情况下,体液和机械信号增加导致血管壁增厚和血管张力增加,这在高血压的发病机制和维持中起重要作用。本综述讨论了高血压血管调节细胞和分子机制理解方面的最新进展。