Mooij J J
Eur J Pharmacol. 1976 Jul;38(1):157-63. doi: 10.1016/0014-2999(76)90212-0.
The effect was measured of low chloride medium and ouabain on carbachol- and acetylcholine-induced depolarizations in denervated rat diaphragm. Membrane potentials were measured in rat diaphragm muscle fibers 10-14 days after denervation. Depolarizations induced by carbachol and acetycholine were increased when the extracellular chloride concentration was diminished from 110 to 40 or 10 mM. Sodium pump inhibition by ouabain (10(-4) M) dramatically enhanced the carbachol depolarizations. In 40 mM Cl- solutions, dose-response relations were determineed with ACh in the absence of presence of dTc. For ACh a pD2 value of 5.2 was found; the pA2 value for dTC appeared to be about 6.4. Therefore, the binding properties of the post-denervational receptors do not appear to be influenced by the chloride gradient. It was concluded that drug-induced depolarizations of the denervated rat diaphragm are short-circuited by chloride ions and counteracted by sodium pumping.
研究了低氯培养基和哇巴因对去神经大鼠膈肌中卡巴胆碱和乙酰胆碱诱导的去极化作用。在去神经后10 - 14天测量大鼠膈肌肌纤维的膜电位。当细胞外氯浓度从110 mM降至40 mM或10 mM时,卡巴胆碱和乙酰胆碱诱导的去极化作用增强。哇巴因(10(-4) M)抑制钠泵可显著增强卡巴胆碱诱导的去极化作用。在40 mM Cl-溶液中,在有无筒箭毒碱(dTc)的情况下测定了乙酰胆碱(ACh)的剂量反应关系。对于ACh,发现pD2值为5.2;dTC的pA2值似乎约为6.4。因此,去神经后受体的结合特性似乎不受氯梯度的影响。得出的结论是,药物诱导的去神经大鼠膈肌去极化作用被氯离子短路,并被钠泵作用抵消。