Effect of β-blockade and subsequent triiodothyronine administration on human leucocyte Na-K ATPase

We have investigated the effect of β-blockade and β-blockade + triiodothyronine (T₃) administration on ⁸⁶Rb (K) influx and [³H]-ouabain binding by human leucocytes and on plasma potassium concentrations. β-blockade with nadolol (40 mg daily) for five days resulted in a significant decrease in ⁸⁶Rb influx and [³H]-ouabain binding, as well as an increase in plasma potassium concentration. T₃ administration thereafter caused a fall in plasma potassium concentration and an increase in ⁸⁶Rb influx. There was a tendency toward restoration of [³H]-ouabain binding to normal. The fact that β-blockade inhibits ⁸⁶Rb (K) influx and increases plasma potassium concentration implies that endogenous adrenaline exerts a tonic stimulatory effect upon ⁸⁶Rb (K) influx and a suppressive effect on plasma potassium concentrations in vivo. T₃ administration induces an increase in ⁸⁶Rb (K) influx and a fall in plasma potassium concentrations. This suggests that either the effect of T₃ is independent of β-adrenoceptors or that the known increase in β-adrenoceptor population secondary to T₃ administration increases sensitivity to circulating adrenaline in spite of β-blocker administration.