The aims were to study effects of iterative exposures to moderate elevations of local intravascular pressure on arterial/arteriolar stiffness and plasma levels of vasoactive substances. Pressures in the vasculature of an arm were increased by 150 mmHg in healthy men (n=11) before and after a 5-wk regimen, during which the vasculature in one arm was exposed to fifteen 40-min sessions of moderately increased transmural pressure (+65 to +105 mmHg). This vascular pressure training and the pressure-distension determinations were conducted by exposing the subjects arm versus remaining part of the body to differential ambient pressure. During the pressure-distension determinations, venous samples were simultaneously obtained from pressurized and unpressurized vessels. Pressure training reduced arterial pressure distension by 40 ± 23% and pressure-induced flow by 33 ± 30% (p<0.01), but only in the pressure-trained arm, suggesting local adaptive mechanisms. The distending pressure-diameter and distending pressure-flow curves, with training-induced increments in pressure thresholds and reductions in response gains, suggest that the increased precapillary stiffness was attributable to increased contractility and structural remodeling of the walls. Acute vascular pressure provocation induced local release of angiotensin-II (Ang-II) and endothelin-1 (ET-1) (p<0.05), suggesting that these vasoconstrictors limited the pressure distension. Pressure training increased basal levels of ET-1 and induced local pressure release of matrix metalloproteinase 7 (p<0.05), suggesting involvement of these substances in vascular remodeling. The findings are compatible with the notion that local intravascular pressure load acts as a prime mover in the development of primary hypertension.

中文翻译：

---

适应5周间歇性局部血管压力增加；原发性高血压的发生机制有哪些？

目的是研究反复暴露于中等程度的局部血管内压力对动脉/小动脉僵硬度和血管活性物质血浆水平的影响。在进行5周治疗之前和之后，健康男性（n = 11）的手臂血管系统压力增加了150 mmHg，在此期间，一只手臂的血管系统暴露于15次40分钟的中度透壁压力升高（ +65至+105 mmHg）。通过使受试者的手臂与身体其余部位接触不同的环境压力来进行血管压力训练和压力-压力的确定。在压力-膨胀测定期间，同时从加压和未加压的容器中获得静脉样品。压力训练可将动脉压力膨胀减少40±23％，将压力引起的流量减少33±30％（p <0.01），但仅限于压力训练的手臂，提示局部适应机制。扩张的压力直径和扩张的压力-流量曲线，以及训练导致的压力阈值增加和响应增益的降低，表明毛细血管前硬度的增加归因于壁的收缩性和结构重塑。急性血管压力激增诱导血管紧张素II（Ang-II）和内皮素1（ET-1）的局部释放（p <0.05），表明这些血管收缩剂限制了压力膨胀。压力训练增加了ET-1的基础水平，并诱导了基质金属蛋白酶7的局部压力释放（p <0.05），表明这些物质参与了血管重塑。这些发现与以下观点相吻合：局部血管内压力负荷是原发性高血压发展的原动力。