Simon Geza
Department of Medicine, VA Medical Center, Minneapolis, Minnesota 55410, USA.
Am J Hypertens. 2003 Dec;16(12):1074-8. doi: 10.1016/j.amjhyper.2003.07.019.
The two physiologic mechanisms that may be responsible for the adverse cardiovascular effects of long-term high sodium diet without increasing blood pressure (BP) are increased blood flow and increased extracellular sodium concentration. The first dilates arteries, and the second may impact on vascular reactivity and growth. The experimental evidence for these two mechanisms was critically reviewed, distinguishing between the administration of physiologically relevant and potentially toxic doses of dietary sodium. There is evidence that a high sodium diet results in dilatation and reduced distensibility of arteries. There is also evidence for an increase of plasma sodium concentration during a high-sodium diet (2 to 5 mmol/L) that may be sufficient to stimulate vascular reactivity and growth. An increase in transmembrane sodium gradient of vascular muscle and increased affinity of receptors for agonists may be the underlying mechanisms. Further experimental evidence is needed to convince the scientific community that lifelong high sodium intake expedites cardiovascular aging and reduces life expectancy independently of its effect on BP.
长期高钠饮食在不升高血压的情况下可能导致不良心血管效应的两种生理机制是血流量增加和细胞外钠浓度升高。第一种机制使动脉扩张，第二种机制可能影响血管反应性和生长。对这两种机制的实验证据进行了严格审查，区分了给予生理相关剂量和潜在毒性剂量的膳食钠的情况。有证据表明，高钠饮食会导致动脉扩张和顺应性降低。也有证据表明，高钠饮食期间血浆钠浓度会升高（2至5 mmol/L），这可能足以刺激血管反应性和生长。血管平滑肌跨膜钠梯度增加以及受体对激动剂的亲和力增加可能是其潜在机制。需要更多的实验证据来说服科学界，终身高钠摄入会加速心血管衰老并降低预期寿命，且独立于其对血压的影响。
