Effect of beta-blockade and subsequent triiodothyronine administration on human leucocyte Na-K ATPase.
We have investigated the effect of beta-blockade and beta-blockade + triiodothyronine (T3) administration on 86Rb (K) influx and [3H]-ouabain binding by human leucocytes and on plasma potassium concentrations. beta-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 concentration and an increase in 86Rb influx. There was a tendency toward restoration of [3H]-ouabain binding to normal. The fact that beta-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 beta-adrenoceptors or that the known increase in beta-adrenoceptor population secondary to T3 administration increases sensitivity to circulating adrenaline in spite of beta-blocker administration.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D006801:Humans; D007962:Leukocytes / Q000201:enzymology*; D008297:Male; D009248:Nadolol / Q000494:pharmacology; D010042:Ouabain / Q000097:blood; D012413:Rubidium / Q000097:blood; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood*; D014284:Triiodothyronine / Q000494:pharmacology*
D000319:Adrenergic beta-Antagonists; D014284:Triiodothyronine; D009248:Nadolol; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium