Experimental evidence for blood pressure-independent vascular effects of high sodium diet

Abstract 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.