Osol George, Brekke Johan Fredrik, McElroy-Yaggy Keara, Gokina Natalia I
Department of Obstetrics and Gynecology, University of Vermont College of Medicine, Burlington 05405, USA.
Am J Physiol Heart Circ Physiol. 2002 Dec;283(6):H2260-7. doi: 10.1152/ajpheart.00634.2002. Epub 2002 Aug 22.
Myogenic behavior, prevalent in resistance arteries and arterioles, involves arterial constriction in response to intravascular pressure. This process is often studied in vitro by using cannulated, pressurized arterial segments from different regional circulations. We propose a comprehensive model for myogenicity that consists of three interrelated but dissociable phases: 1) the initial development of myogenic tone (MT), 2) myogenic reactivity to subsequent changes in pressure (MR), and 3) forced dilatation at high transmural pressures (FD). The three phases span the physiological range of transmural pressures (e.g., MT, 40-60 mmHg; MR, 60-140 mmHg; FD, >140 mmHg in cerebral arteries) and are characterized by distinct changes in cytosolic calcium (Ca(2+)), which do not parallel arterial diameter or wall tension, and therefore suggest the existence of additional regulatory mechanisms. Specifically, the development of MT is accompanied by a substantial (200%) elevation in Ca(2+) and a reduction in lumen diameter and wall tension, whereas MR is associated with relatively small Ca(2+) increments (<20% over the entire pressure range) despite considerable increases in wall tension and force production but little or no change in diameter. FD is characterized by a significant additional elevation in Ca(2+) (>50%), complete loss of force production, and a rapid increase in wall tension. The utility of this model is that it provides a framework for comparing myogenic behavior of vessels of different size and anatomic origin and for investigating the underlying cellular mechanisms that govern vascular smooth muscle mechanotransduction and contribute to the regulation of peripheral resistance.
肌源性活动在阻力动脉和小动脉中普遍存在,涉及对血管内压力作出反应的动脉收缩。这个过程通常在体外通过使用来自不同区域循环的插管加压动脉段来研究。我们提出了一个关于肌源性的综合模型,该模型由三个相互关联但可分离的阶段组成:1)肌源性张力(MT)的初始发展,2)对随后压力变化的肌源性反应性(MR),以及3)在高跨壁压力下的强制扩张(FD)。这三个阶段涵盖了跨壁压力的生理范围(例如,MT为40 - 60 mmHg;MR为60 - 140 mmHg;脑动脉中的FD > 140 mmHg),其特征是胞质钙(Ca(2 +))有明显变化,这些变化与动脉直径或壁张力不平行,因此表明存在额外的调节机制。具体而言,MT的发展伴随着Ca(2 +)大幅升高(200%)以及管腔直径和壁张力降低,而MR与相对较小的Ca(2 +)增量相关(在整个压力范围内< 20%),尽管壁张力和力的产生有相当大的增加,但直径几乎没有变化或没有变化。FD的特征是Ca(2 +)显著进一步升高(> 50%)、力的产生完全丧失以及壁张力迅速增加。这个模型的作用在于它提供了一个框架,用于比较不同大小和解剖来源的血管的肌源性活动,并用于研究控制血管平滑肌机械转导并有助于调节外周阻力的潜在细胞机制。