There are two fractions of sodium in the arterial wall which can be selectively and reversibly exchanged for other ions. These fractions are believed to be bound to the acid mucopolysaccharide – protein component of the paracellular matrix. The first fraction seems to be loosely bound by weakly acidic groups, probably the carboxyl groups of the hexuronic acid moieties. It can be exchanged for hydrogen even in neutral solutions by reducing the concentration of sodium ions in the medium. In the rat tail artery, the average size of this fraction did not exceed 0.5 meq/100 g of dry fat-free tissue. The second fraction behaves as if it is more tightly bound, apparently by strongly acidic groups like the sulfo groups of the mucopolysaccharides. It amounts to 2.21 ± 0.20 meq/100 g of dry fat-free tissue if a simplified system of sodium and calcium chloride solutions is used. In the presence of normal plasma concentrations of potassium and magnesium, the sum of both sodium fractions is increased substantially and is equal to approximately 5 meq/100 g of dry fat-free tissue. This bound sodium is increased in arteries of immature animals and animals with established DOCA hypertension, both of which have a higher content of the acid mucopolysaccharides.

Viable tail artery samples, in a modified Krebs medium, gain Na in exchange for K during cooling and reverse the process during rewarming. The process, within the margin of experimental error, is usually in a 1:1 ratio and has a long time constant, about 8 to 9 meq/100 g dry weight being exchanged within 3 h of cooling, and up to 15 meq/100 g within 24 h. Three hours of rewarming of tissues prepared by overnight (18 h) cooling is sufficient for an exchange of at least 10 meq/100 g. A second component of Na, equal to approximately 10 meq/100 g in tissue incubated in a Tris-buffered medium [Formula: see text], is apparently paracellular, for it is fully mobilized within 30 min of exposure to a sodium-free environment, even at 2°. Since even 3 h of exposure to such a medium at 2° fails to mobilize metabolism-dependent cellular Na it is possible to differentiate these two components. Evidence is also presented to show that Na transport, ordinarily associated with K accumulation, can occur without it.

The ionic composition of the incubated rat tail artery, comparable but not identical to that of the freshly dissected tissue, can be maintained over a period of at least 5 h under aerobic conditions in the absence of utilizable exogenous substrate. A sufficient supply of exogenous glucose must be provided for the maintenance of this ionic composition under anaerobic conditions. The changes in the content of individual ions and water brought about by iodoacetate poisoning can be prevented more or less completely by addition of a utilizable noncarbohydrate substrate such as pyruvate or butyrate to the incubation medium. Abolition of the transmembrane ionic gradients caused by 2,4-dinitrophenol or oligomycin can be partially-prevented by exogenous glucose. The ionic composition of the artery is little affected by fluoroacetate inhibition even in the absence of utilizable exogenous substrate. The content of magnesium is decreased by 2-deoxy-D-glucose, although the content of other ions remains unchanged. Metabolic energy seems to be required to prevent the tissue calcium from rising.

There is a statistically significant positive correlation between the total water content of the arterial wall and the concentration of sodium bound to negatively charged groups of the protein–polysaccharide gel. The fraction of water associated with the protein–polysaccharide gel is located almost exclusively in the inulin space, and is significantly increased in hypertension. The size of this fraction can be reduced by exchanging sodium—the main counterion under physiological conditions—for a divalent ion. There is no difference between calcium and magnesium in this regard. The configuration of the gel, which is given primarily by the relative concentration of the charged groups and the valency of the counterion, determines the size of the inulin space.

The distribution of Na, K, and water in the rat tail artery was studied with a view to further characterizing the distribution of Na within the inulin-inaccessible phase of a typical small artery. Two components of Na can be demonstrated by rewarming precooled, Na-loaded arteries. One component is liberated within minutes of rewarming, unassociated with any K exchange and unaffected by iodoacetate blockade. The larger component is liberated slowly over hours, usually associated 1:1 with the converse movement of K and metabolically driven. The metabolic extrusion of Na can proceed, however, even if K influx is blocked.