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The neuromuscular transmission fade (Wedensky inhibition) induced by L-arginine in neuromuscular preparations from rats.

机译:L-精氨酸在大鼠神经肌肉制剂中引起的神经肌肉传递衰减(Wedensky抑制)。

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摘要

L-Arginine (4.7-18.8 mM) and 3-(4-morpholinyl)-sydonone imine hydrochloride (SIN-1; 1.15 mM) induced an increase in tetanic fade caused by indirect stimulation (180-200 Hz) of muscle. However, Wedensky inhibition, different from control, was not observed when the preparations treated with d-tubocurarine were directly stimulated by the same frequency. D-Arginine (9.4 mM) was ineffective in changing R values caused by indirect stimulation (180-200 Hz) of muscle. N(omega)-Nitro-L-arginine (73 mM) or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM) did not produce any effect on Wedensky inhibition but did antagonize the tetanic fade induced by L-arginine (9.4 mM). The SIN-1 effect was antagonized by previous administration of ODQ (108 microM), which alone did not produce any effects on R values. These results indicate that NO acting at the presynaptic level increases the Wedensky inhibition induced by high frequency of stimulation applied on motor nerves, and its effect may be produced through the cGMP-GC pathway.
机译:L-精氨酸(4.7-18.8 mM)和3-(4-吗啉基)-sydonone亚胺盐酸盐(SIN-1; 1.15 mM)诱导了肌肉的间接刺激(180-200 Hz)引起的破伤风褪色增加。然而,当以相同频率直接刺激用d-微管尿素处理的制剂时,未观察到与对照不同的Wedensky抑制作用。 D-精氨酸(9.4 mM)在改变由肌肉间接刺激(180-200 Hz)引起的R值方面无效。 N(ω)-硝基-L-精氨酸(73 mM)或1H- [1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one(ODQ; 10 microM)对Wedensky不产生任何影响抑制,但确实拮抗了L-精氨酸(9.4 mM)诱导的强直性衰落。以前施用ODQ(108 microM)可以拮抗SIN-1的作用,单独使用ODQ不会对R值产生任何影响。这些结果表明,在突触前水平起作用的NO增加了由施加在运动神经上的高频率刺激引起的Wedensky抑制作用,其作用可能是通过cGMP-GC途径产生的。

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