Role of adrenoceptors and cAMP on the catecholamine-induced inhibition of proteolysis in rat skeletal muscle.
The role of adrenoceptor subtypes and of cAMP on rat skeletal muscle proteolysis was investigated using a preparation that maintains tissue glycogen stores and metabolic activity for several hours. In both soleus and extensor digitorum longus (EDL) muscles, proteolysis decreased by 15-20% in the presence of equimolar concentrations of epinephrine, isoproterenol, a nonselective beta-agonist, or clenbuterol, a selective beta(2)-agonist. Norepinephrine also reduced proteolysis but less markedly than epinephrine. No change in proteolysis was observed when muscles were incubated with phenylephrine, a nonselective alpha-agonist. The decrease in the rate of protein degradation induced by 10(-4) M epinephrine was prevented by 10(-5) M propranolol, a nonselective beta-antagonist, and by 10(-5) M ICI 118.551, a selective beta(2)-antagonist. The antiproteolytic effect of epinephrine was not inhibited by prazosin or yohimbine (selective alpha(1)-and alpha(2)-antagonists, respectively) or by atenolol, a selective beta(1)-antagonist. Dibutyryl cAMP and isobutylmethylxanthine reduced proteolysis in both soleus and EDL muscles. The data suggest that catecholamines exert an inhibitory control of skeletal muscle proteolysis, probably mediated by beta(2)-adrenoceptors, with the participation of a cAMP-dependent pathway.
Navegantes
L C
LC
Department of Physiology and Biochemistry, School of Medicine, University of São Paulo, Ribeirão Preto, Brazil.
Resano
N M
NM
Migliorini
R H
RH
Kettelhut
I C
IC
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002395:Catecholamines / Q000494:pharmacology*; D000242:Cyclic AMP / Q000502:physiology*; D006003:Glycogen / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009124:Muscle Proteins / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D009124:Muscle Proteins; D010726:Phosphodiesterase Inhibitors; D011941:Receptors, Adrenergic; D010725:Phosphocreatine; D003994:Bucladesine; D000255:Adenosine Triphosphate; D006003:Glycogen; D000242:Cyclic AMP; D015056:1-Methyl-3-isobutylxanthine