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Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine London, United Kingdom
Address all correspondence and requests for reprints to: Dr. P. Dandona, Metabolic Unit, Department of Chemical Pathology and Human Metabolism, Royal Free Hospital, Pond Street, London, NW3 2QG United Kingdom.
The effect of short term T3 administration on leukocyte ouabain-sensitive 86Rb(K) influx and Na efflux in normal subjects was investigated. At a dose of 60 µg daily for 7 days, T3 induced a significant increase in leukocyte 86Rb(K) influx and a significant fall in plasma K concentrations. Plasma and intracellular Na concentrations did not change. [3H]Ouabain binding, a measure of Na-K ATPase units, did not change. A week after T3 administration, 86Rb(K) influx, Na efflux, and plasma K concentrations were normal. In a series of five hyperthyroid patients, both ouabain-sensitive 86Rb influx and [3H] ouabain binding were significantly greater than in normal subjects. We conclude that T3 stimulates 86Rb(K) influx and Na efflux by leukocytes in vivo independently of [3H]ouabain binding and that this increase is rapidly reversible. However, in hyperthyroid patients both 86Rbinflux and [3H] ouabain binding are increased, probably due to prolonged exposure to thyroid hormone excess.
* Supported by a fellowship from the government of Iraq.
Received May 5, 1987.
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