The effect of beta-receptor blockade on adrenaline-induced changes in redox and energy state in m. vastus lateralis and m. soleus of the rat in vivo.
The metabolic changes in blood, red (m. soleus) and white (m. vastus lateralis) skeletal muscle fibres were investigated after short-term (3 min) infusion of adrenaline with or without prior treatment with propranolol or metoprolol. The adrenaline-induced increase in plasma lactate levels was totally prevented by prior treatment with metoprolol or propranolol, whilst the beta-blockers had no effect on blood glucose levels. Similar effects on lactate levels were found in the m. soleus, while metoprolol was less effective than propranolol in m. vastus lateralis. Adrenaline decreased the level of muscle creatinine phosphate and ADP, causing the equilibrium of the creatinine kinase reaction to change in the direction of ATP synthesis, although the level of ATP usually decreased. This effect was more pronounced in m. vastus lateralis compared with m. soleus. The [ATP]/[ADP] [Pi]-ratio tended to increase during infusion of adrenaline. This effect was counteracted by metroprolol but not by propranolol. The effects on the "phosphate potential" ([ATP]/[ADP] [Pi]) and the equilibrium within the creatine kinase were more pronounced in m. vastus lateralis than in m. soleus. The results demonstrate the possible role of receptors other than beta-receptors, i.e. alpha-receptors, in mediating changes in plasma glucose levels, while plasma lactate levels are regulated by the beta-adrenergic system. The role of beta-receptors in mediating changes in muscle lactate levels may differ in m. soleus and m. vastus lateralis, with a relative predominance of beta 2-receptors in m. vastus lateralis. Quantitative and qualitative differences in the adrenergic control of the energy state in the two types of muscle fibre were obvious, although it was not possible to distinguish clearly between the relative importance of alpha, beta 1 and beta 2-receptors.
D000227:Adenine Nucleotides / Q000032:analysis; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003401:Creatine / Q000032:analysis; D004734:Energy Metabolism / Q000187:drug effects*; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006003:Glycogen / Q000032:analysis; D007773:Lactates / Q000032:analysis; D008790:Metoprolol / Q000494:pharmacology; D009132:Muscles / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D010710:Phosphates / Q000032:analysis; D010725:Phosphocreatine / Q000032:analysis; D011433:Propranolol / Q000494:pharmacology; D011773:Pyruvates / Q000032:analysis; D051381:Rats
D000227:Adenine Nucleotides; D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D007773:Lactates; D010710:Phosphates; D011773:Pyruvates; D010725:Phosphocreatine; D006003:Glycogen; D011433:Propranolol; D008790:Metoprolol; D003401:Creatine; D004837:Epinephrine