The stimulating effect of adrenaline on active electrogenic Na-K-transport in rat soleus muscle is mediated primarily by beta-2 adrenoceptors.
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Rat muscle data on beta-2 Na-K effects do not inform practice; leaves open human translation and cardiac relevance.
The relative role of beta 1- and beta 2-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 (EM) 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 beta 1-selective adrenoceptor antagonist, metoprolol, was found to be at least 50 times less potent. 4 The beta 2-adrenoceptor agonist, salbutamol, was at least 100 times as potent as H133/22 (a beta 1-selective agonist) in stimulating 22Na-efflux and 42K-influx. 5 In experiments performed under pentobarbitone anaesthesia, the intravenous injection of adrenaline (5 microgram) or salbutamol (0.5 to 50 microgram) led to a rapid and marked increase in the EM of the exposed soleus muscle. This hyperpolarizing effect could not be accounted for by the concomitant, relatively modest change in extracellular K.
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Clausen et al. (1980) studied this question.
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