Lithium substitution and the distribution of sodium in the rat tail artery.

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.