α-肾上腺素能激动剂对原位脂肪细胞线粒体膜电位的影响。
The effect of alpha-adrenergic agonists on the membrane potential of fat-cell mitochondria in situ.
作者信息
Davis R J, Martin B R
出版信息
Biochem J. 1982 Sep 15;206(3):619-26. doi: 10.1042/bj2060619.
Abstract
- The accumulation of [3H]methyltriphenylphosphonium by isolated fat-cells was used to estimate the membrane potential of mitochondria in situ. 2. An alpha-adrenergic receptor-mediated decrease in the apparent accumulation of [3H]methyltriphenylphosphonium was observed. Methoxamine, clonidine and low concentrations of phenylephrine decreased the calculated mitochrondrial membrane potential without significantly raising cyclic AMP levels, adenylate cyclase activity or stimulating lipolysis. The agonist potency order was phenylephrine greater than methoxamine greater than clonidine. 3. The decrease in the calculated mitochondrial membrane potential caused by phenylephrine, clonidine and methoxamine was blocked by the alpha-adrenergic antagonist prazosin but not by yohimbine nor by the beta-antagonist propranolol. This suggests that the effect on the calculated mitochondrial membrane potential may be mediated by alpha 1-like receptors.
摘要
- 利用分离的脂肪细胞对[3H]甲基三苯基鏻的摄取来估算线粒体在原位的膜电位。2. 观察到α-肾上腺素能受体介导的[3H]甲基三苯基鏻表观摄取量减少。甲氧明、可乐定和低浓度的去氧肾上腺素降低了计算得出的线粒体膜电位，而未显著提高环磷酸腺苷水平、腺苷酸环化酶活性或刺激脂肪分解。激动剂效力顺序为去氧肾上腺素大于甲氧明大于可乐定。3. 去氧肾上腺素、可乐定和甲氧明引起的计算得出的线粒体膜电位降低被α-肾上腺素能拮抗剂哌唑嗪阻断，但未被育亨宾或β-拮抗剂普萘洛尔阻断。这表明对计算得出的线粒体膜电位的影响可能由α1样受体介导。
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