No abstract

SUMMARY1. The relation between [Mg]. and the Mg content of the rat tail artery incubated in Ca-free solutions was studied.2. Variation of [Mg]. in Ca-free Krebs solution between 0-6 and 2-4 mm did not affect the cell Mg. In ATP-depleted arteries, a sizeable fraction of the cell Mg was found to be proportional to [Mg] 6. The results are consistent with the hypothesis that the outwardly directed Mg pump in rat vascular smooth muscle utilizes the energy released in the course of spontaneous influx of Na.

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.

Capillary glass electrodes were used in two separate procedures to examine the kinetics of exchange of Na+ for K+ during rewarming of the precooled rat tail artery. In the first system, the intravascular medium remains stationary in the artery for intervals of 3, 6, or 9 min, and the change in ion concentrations in this small volume (approximately 25 × 10−3 ml) is then measured by difference against a parallel "dummy" system. In the second procedure, the intravascular medium moves continuously at 0.01 ml/min and is collected in fine bore polyethylene tubing for later passage through the electrodes at 0.15 ml/min. Both systems yielded similar quantitative data but the first system was less precise and it is possible that the artery was less well maintained. The second system clearly revealed an extra complement of Na+ liberated from the tissue well in advance of an observable, metabolically driven uptake of K+ and provided a detailed substantiation of previously reported deductions of this fact. The final equilibrium transcellular Na+ and K+ gradients attained after rewarming were lower in stretched than in unstretched arteries.

The total activity of pyruvate dehydrogenase (EC 1.2.4.1) and the fraction of the enzyme in the active form were assayed in brown fat and liver throughout the development of the rat. In brown adipose tissue, the total activity increased until the late suckling period. After weaning, a decrease was noted. The fraction of the enzyme in the active form did not increase until after 10 days of age, reached its highest level in the late suckling period and remained at this level after weaning. Pyruvate dehydrogenase in liver decreased in both total activity and percentage activity in the early neonatal period. Both parameters increased after this period, reaching their highest levels in the late suckling period. In both fetal liver and fetal brown fat, the total activity of pyruvate dehydrogenase was increased by in vitro incubation with insulin.