New insights into salt-sensitive hypertension

Salt sensitivity, described as association between salt intake and blood pressure, varies among individuals. HSD contributes to salt-sensitive hypertension. Traditional view on blood pressure regulation was focused on the kidneys and ECV expansion secondary to body Na+ load. However, the latest data suggest that salt-sensitive hypertension does not primarily come about by volume-related mechanisms and other than the renal body fluid control must play an important role. Since Na+ accumulation in the body does not necessarily lead to expansion of the extracellular volume it is suggested that Na+ might be stored in an osmotically inactive form either as osmotically inactive Na+ storage in the skin and/or osmotically neutral Na+/K+ exchange in muscle. Hypertonicity in the skin interstitium compared with blood and therefore osmotic stress may be a crucial cause of interstitial Na+ accumulation and hypertension development. Dietary salt loading increases osmotically inactive skin Na+ storage and polyanionic character of the skin, leading to local hypertonicity. The response to this hypertonic internal environment in the skin interstitium involves MPS-driven and TonEBP-VEGF-C-mediated hyperplasia of lymph capillaries and increased eNOS expression. A decreased osmotically inactive storage capacity for Na+ or reduced osmotically neutral Na+/K+ exchange may predispose to marked volume retention, and therefore to rise in blood pressure.