β2‐ADRENOCEPTORS MEDIATE THE STIMULATING EFFECT OF ADRENALINE ON ACTIVE ELECTROGENIC NA‐K‐TRANSPORT IN RAT SOLEUS MUSCLE

Abstract

1 The relative role of β₁- and β₂-adrenoceptors in mediating the stimulating effect of adrenaline on active electrogenic Na-K-transport has been assessed in experiments on rat soleus muscles in vitro and in vivo. 2 In the rat isolated soleus muscle, adrenaline (10⁻⁶ m) increases the resting membrane potential (E_M) by 5.8 mV and stimulates ²²Na-efflux and ouabain-suppressible ⁴²K-uptake by 91 and 94%, respectively. 3 All of these effects are completely blocked by propranolol (10⁻⁵ m), whereas the β₁,-selective adrenoceptor antagonist, metoprolol, was found to be at least 50 times less potent. 4 The β₂-adrenoceptor agonist, salbutamol, was at least 100 times as potent as H133/22 (a β₁-selective agonist) in stimulating ²²Na-efflux and ⁴²K-influx. 5 In experiments performed under pentobarbitone anaesthesia, the intravenous injection of adrenaline (5 μg) or salbutamol (0.5 to 50 μg) led to a rapid and marked increase in the E_M of the exposed soleus muscle. This hyperpolarizing effect could not be accounted for by the concomitant, relatively modest change in extracellular K.