Akaike N, Hirata A, Kiyohara T, Oyama Y
J Physiol. 1983 Aug;341:245-55. doi: 10.1113/jphysiol.1983.sp014804.
C.N.S.-induced suppression of muscle Na-pump activity was studied in fast 'twitch' muscle, extensor digitorum longus, of hypokalaemic rats which were fed a K-deficient diet for 0-9 weeks. The results were compared with those of slow 'tonic' muscle, soleus, reported previously. K-deficient diet caused blood hypokalaemia and a considerable K+ loss and Na+ accumulation in the skeletal, heart and smooth muscles. The cellular K+ loss was in the order of soleus greater than extensor digitorum longus greater than diaphragm greater than duodenum greater than auricle greater than ventricle; C.N.S. organs such as cerebrum, cerebellum, medulla oblongata, spinal cord and liver were spared this K+ fall. Skeletal, heart and smooth muscles lost more K+ with prolongation of hypokalaemic periods, whereas plasma K+ concentration did not fall much below 1.6 mM during hypokalaemia. Peripheral nerve section, cervical and brain-stem transection, decerebration and cortical spreading depression with 20% KCl, which activated the active Na+ and K+ transport in soleus muscles during hypokalaemia, could not enhance the pump activity in extensor digitorum longus muscles. Alpha-adrenoreceptor antagonists such as phenoxybenzamine, phentolamine and dibenamine and a specific blocker of post-synaptic alpha 1-adrenoreceptor, prazosin, did not stimulate Na+ and K+ transport in the extensor digitorum longus muscles during hypokalaemia while the beta-adrenoreceptor antagonist, propranolol, also had no effect. The sensitivity of the active Na+ and K+ transport system in rat muscles to ouabain applied intraperitoneally was greater in extensor digitorum longus muscles than in soleus muscles. The binding experiment with a radiolabelled ligand of alpha 1 adrenoreceptor antagonist, [3H]prazosin, demonstrated the presence of alpha 1-adrenergic receptors on the soleus muscle membranes of hypokalaemic rats, but not of normal rats. alpha 1 Adrenergic receptors were not detected on the extensor digitorum longus muscle membranes prepared from either hypokalaemic or normal rats. The correlation between the C.N.S.-induced inhibition on the Na pump in soleus muscle during hypokalaemia and the occurrence of alpha 1 adrenergic receptors on the muscle was discussed.
在低钾血症大鼠的快“抽动”肌（趾长伸肌）中研究了中枢神经系统（C.N.S.）诱导的肌肉钠泵活性抑制情况，这些大鼠食用低钾饮食0 - 9周。将结果与先前报道的慢“紧张性”肌（比目鱼肌）的结果进行了比较。低钾饮食导致血液低钾血症以及骨骼肌、心肌和平滑肌中大量钾离子流失和钠离子蓄积。细胞内钾离子流失的顺序为：比目鱼肌＞趾长伸肌＞膈肌＞十二指肠＞心耳＞心室；大脑、小脑、延髓、脊髓和肝脏等中枢神经系统器官未出现这种钾离子下降情况。随着低钾血症持续时间延长，骨骼肌、心肌和平滑肌流失更多钾离子，而低钾血症期间血浆钾离子浓度不会降至1.6 mM以下太多。外周神经切断、颈髓和脑干横断、去大脑以及用20%氯化钾进行皮质扩散性抑制，这些操作在低钾血症期间能激活比目鱼肌中的活性钠钾转运，但不能增强趾长伸肌中的泵活性。α - 肾上腺素能受体拮抗剂如酚苄明、酚妥拉明和二苄明以及突触后α1 - 肾上腺素能受体的特异性阻滞剂哌唑嗪，在低钾血症期间不会刺激趾长伸肌中的钠钾转运，而β - 肾上腺素能受体拮抗剂普萘洛尔也无作用。大鼠肌肉中活性钠钾转运系统对腹腔注射哇巴因的敏感性，趾长伸肌大于比目鱼肌。用放射性标记的α1肾上腺素能受体拮抗剂[3H]哌唑嗪进行的结合实验表明，低钾血症大鼠的比目鱼肌膜上存在α1 - 肾上腺素能受体，而正常大鼠则没有。在低钾血症或正常大鼠制备的趾长伸肌膜上均未检测到α1肾上腺素能受体。讨论了低钾血症期间中枢神经系统对比目鱼肌钠泵的诱导抑制与肌肉上α1肾上腺素能受体出现之间的相关性。
