Schadewaldt P, Stapper N J, Staib W
FEBS Lett. 1987 Jun 8;217(1):45-8. doi: 10.1016/0014-5793(87)81239-5.
Adrenergic regulation of phosphoinositide breakdown in rat skeletal muscle was investigated in 30-min incubations with 10 mM LiCl. In rat hemidiaphragms, prelabelled with D-myo-[2-3H]inositol, addition of alpha-agonists (epinephrine, norepinephrine, phenylephrine) induced a 5-8-fold increase of [3H]inositol monophosphate accumulation. This could be prevented by inclusion of alpha-antagonists (phentolamine, prazosin). beta-Agonists and/or beta-antagonists had no effect. Similar experiments with isolated flexor digitorum brevis muscle fibers yielded confirmatory results. Functional integrity of beta-receptor mediated processes was suggested by the beta-agonist-induced increase of glucose 6-phosphate in hemidiaphragms and cAMP in fiber preparations. The results indicate that phosphoinositide breakdown in differentiated rat skeletal muscle is, at least in part, under alpha-adrenergic control.
在含有10 mM LiCl的30分钟孵育实验中,研究了大鼠骨骼肌中磷酸肌醇分解的肾上腺素能调节。在用D-肌醇-[2-3H]肌醇预标记的大鼠半横膈中,添加α-激动剂(肾上腺素、去甲肾上腺素、苯肾上腺素)会导致[3H]肌醇单磷酸积累增加5至8倍。这可以通过加入α-拮抗剂(酚妥拉明、哌唑嗪)来预防。β-激动剂和/或β-拮抗剂没有效果。对分离的趾短屈肌纤维进行的类似实验也得到了证实性结果。β-激动剂诱导半横膈中6-磷酸葡萄糖增加以及纤维制剂中cAMP增加,提示β-受体介导过程的功能完整性。结果表明,分化的大鼠骨骼肌中的磷酸肌醇分解至少部分受α-肾上腺素能控制。