Is intracellular sodium increased in hypertension?

It is generally assumed that the intracellular Na+ content (Nq)* of vascular smooth muscle is increased in essential hypertension and several experimental models of hypertension [l, 21. The assumption dates back to the original reports of increased Na+ content of arteries in human and experimental hypertension by Tobian [3]. Based on the finding of an elevated arterial wall Na+/Clratio, he concluded that some of the excess Na+ was intracellular. However, an increased Na+/Clratio is also compatible with the accumulation of excess cation-binding glycosaminoglycans in the extracellular matrix of arteries. Indeed, in dogs with hypertension secondary to coarctation of the aorta, Hollander et al. [4] found that the glycosaminoglycan content of the 'hypertensive' portion of the thoracic aorta was increased and might have been the factor directly responsible for the accumulation of excess Na+ [4]. Extracellular bound Na+ was found to be increased also in the tail artery of rats with deoxycorticosterone acetate (D0CA)-salt and two-kidney, one-clip (2K,lC) hypertension [5,6].