Kinetic studies on the stimulation of Na+−H+ exchange activity in renal brush border membranes isolated from thyroid hormone-treated rats

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Abstract
Na+−H+ exchange activity in renal brush border membrane vesicles isolated from hyperthyroid rats was increased. When examined as a function of [Na+], treatment altered the initial rate of Na+ uptake by increasingV m (hyperthyroid, 18.9±1.1 nmol Na+ · mg−1 · 2 sec−1; normal, 8.9±0.3 nmol Na+ · mg−1 · 2 sec−1), and not the apparent affinityK Na + (hyperthyroid, 7.3±1.7mm; normal, 6.5±0.9mm). When examined as a function of [H+] and at a subsaturating [Na+] (1mm), hyperthyroidism resulted in the proportional increase in Na+ uptake at every intravesicular pH measured. A positive cooperative effect on Na+ uptake was found with increased intravesicular acidity in vesicles from both normal and hyperthyroid rats. When the data were analyzed by the Hill equation, it was found that hyperthyroidism did not change then (hyperthyroid, 1.2±0.06; normal, 1.2±0.07) or the [H+]0.5 (hyperthyroid, 0.39±0.08 μm; normal, 0.44±0.07 μm) but increased the apparentV m (hyperthyroid, 1.68±0.14 nmol Na+ · mg−1 · 2 sec−1; normal 0.96±0.10 nmol Na+ · mg−1 · 2 sec−1). The uptake of Na+ in exchange for H+ in membrane vesicles from normal and hyperthyroid animals was not influenced by membrane potential. H+ translocation or debinding was rate limiting for Na+−H+ exchange since Na+−Na+ exchange activity was greater than Na+−H+ exchange activity. Hyperthyroidism caused a proportional increase and hypothyroidism caused a proportional decrease in Na+−Na+ and Na+−H+ exchange. We conclude that hyperthyroidism leads to either an increase in the number of functional exchangers in the membrane or exactly proportional increases in the rate-limiting steps for Na+−Na+ and Na+−H+ exchange activity.