Modulating influence of D,L-propranolol on triiodothyronine-induced skeletal muscle protein degradation.
There is evidence suggesting that thyrotoxicosis increases beta-adrenoreceptor density on some target tissues. We have studied the in vivo effect of D,L-propranolol (a nonselective beta-adrenoreceptor blocking agent) on T3-induced enhancement of in situ proteolysis in fast twitch muscle fibers of the rat. Chronic treatment with T3 as opposed to saline resulted in a 76% enhancement of the rate of in situ muscle proteolysis [0.79 +/- 0.04 (n = 8) compared with 0.45 +/- 0.01 (n = 8) nmol tyrosine/mg muscle . 2 h]. Treatment of rats with both T3 and 2 mg propranolol resulted in a 62% reduction in the T3-induced increment in situ muscle proteolysis [0.58 +/- 0.02 (n = 8) vs. 0.79 +/- 0.04]. This significant inhibition by propranolol of T3-induced enhanced proteolytic rates in vitro suggests that this may comprise one component of the observed beneficial clinical effects of beta-blockade in thyrotoxic myopathy.
D000818:Animals; D001835:Body Weight; D004347:Drug Interactions; D002149:Energy Intake; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism*; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000494:pharmacology*
D009124:Muscle Proteins; D014284:Triiodothyronine; D011433:Propranolol; D013974:Thyroxine