The exchange of lithium (Li) with sodium (Na) was explored in an effort to quantify cellular Na in the rat tail artery. Two phases of cellular Na were demonstrated by the kinetics of exchange at 37°C. Cellular Na, was rapidly lost following cell disruption and increased in proportion to potassium (K) loss during conventional Na enrichment in a Kfree medium. Cooling to 2°C almost abolished the transmembrane movement of Li; therefore, a simple 30-minute incubation in cold Li medium removed extracellular but not cellular Na. To prove that the residual Na after such a wash in cold Li was cellular, we demonstrated that Na exchanges readily with Li even at 2°C after cells are disrupted, increases slowly in proportion to K loss during prolonged cooling, and increases rapidly in a precise one-to-one ratio with K loss when active Na transport is stopped by incubation in a K-free medium. Cellular Na in the normal artery was about 20-25 mmoles/kg dry weight when cellular K was about 225 mmolesAg dry weight. In arteries from rats with deoxycorticosterone acetate-induced hypertension of 8 weeks duration, a 13% fall in cellular K was balanced one to one by an increase in cellular Na.

The tail artery of the spontaneously hypertensive rat (SHR) (Carworth Farms), excised rapidly and immersed immediately in cold (2 degrees C) Li-substituted physiologic salt solution (LiPSS), continues to exchange cell Na+ and K+ for Li+, this exchange is negligible to the control (Carworth Farms normotensive) CFN). In the incubated artery at 37 degrees C, when the vascular smooth muscle cell is slack, the leakiness of the cell membrane in the SHR is more than offset by increased Na+ pumping activity, so that cell Na+ is subnormal. A high precision technique with ion-specific electrodes was developed to follow the passive downhill and active uphill phases of Na+-K+ exchange in the perfused artery exposed to K+-free physiologic salt solution (K+-free PSS) followed by physiological salt solution (PSS). The exchange was found to be fully reversible and sufficiently equimolar to be definable in terms of movements of K+ alone. The rates of ionic movement across the vascular smooth muscle cell were found to be about 6 times faster for the vessel perfused at low pressure (less than 3 mm Hg) than for the slack incubated artery. The rate of passive downhill movement was significantly accelerated in the mature SHR compared with CFN, and the net active transport activity much enhanced. Similar changes were seen as early as 3 weeks after treatment with DOCA and were pronounced at 8 weeks. It is proposed that conditions favoring a sustained accumulation of Na+ in the vascular smooth muscle cell are countered by an enhanced synthesis of transport protein, of contractile protein, and of paracellular matrix protein which progressively restructure the wall.

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Cell Na in the rat tail artery was measured by replacing all extracellular Na with Li at 2°C. Water was partitioned with ¹⁴C-sorbitol as the marker. The binding capacity of the cytoplasm was estimated by ion-exchange after the destruction of cell membranes by alternate freezing and thawing. Cell Na is of the order of 20–25 mEq/kg dry weight and about ²/₃ of this may be in free solution with [Na]_i in the range of 15 mEq/liter. Cell K is about 220 mEq/kg dry weight and, of this, 30 mEq or more is bound so that [K]_i is not greater than 190 mEq/liter. These estimates allow only for the low figure of 30 mEq as the sum of site-bound cell monovalent cations. It is shown, however, that as much as 50-60 mEq may be site-bound or otherwise restricted within the cell. A similar amount, mostly Na⁺, is site-bound within the paracellular matrix.