Sodium Handling by the Blood Vessel Wall

Abstract

Extensive research has focused on the association between high-sodium intake and hypertension. New ideas about sodium homeostasis decisively influence the existing ideas about this association. Classically, according to the 2-compartment model, sodium particularly accumulates in the extracellular space, where it equally divides between the intravascular and the interstitial compartment. This is followed by commensurate water retention to maintain normal osmolality. The consequent increase in extracellular volume was considered to be the main causative factor for hypertension. However, consecutive studies revealed that increases in sodium load were neither accompanied by the expected increases in total body water or body weight nor could be accounted for by the excreted amounts of sodium in the urine.1–3 In other words, sodium was missing. Accordingly, the existence of nonosmotic sodium buffers was suggested.3 In this review, we will speculate on the implications of this missing sodium with regard to blood pressure regulation by discussing the journey that sodium undertakes from the circulation and state that sodium handling by the blood vessel wall seems crucial in the development and prevention of hypertension. Two meticulously performed balance studies in 2000 and 2002 were the first to point out that something was amiss in the common view about sodium homeostasis. In 2000, Heer et al2 revealed that, in contrast to the common thought, an increase in body sodium induced by high-sodium diet was not paralleled by an increase in total body water. Subsequently, Titze et al3 executed a long-term study of 135 days in healthy volunteers who were confined to spaceflight stimulating conditions. Sodium and other electrolyte intake were carefully monitored. Toward the end of the study, sodium gain exceeded weight gain, which introduced the possibility of a nonosmotic sodium storage compartment. A few years later, this hypothesis was confirmed, as rats …