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钙离子浓度和钙离子通道阻滞剂对大鼠尾动脉去甲肾上腺素释放及嘌呤能神经效应传递的影响

Effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline release and purinergic neuroeffector transmission in rat tail artery.

作者信息

Brock J A, Cunnane T C

机构信息

Prince of Wales Medical Research Institute, Randwick, NSW, Australia.

出版信息

Br J Pharmacol. 1999 Jan;126(1):11-8. doi: 10.1038/sj.bjp.0702256.

Abstract
  1. The effects of Ca2+ concentration and Ca2+ channel blockers on noradrenaline (NA) and adenosine 5'-triphosphate (ATP) release from postganglionic sympathetic nerves have been investigated in rat tail arteries in vitro. Intracellularly recorded excitatory junction potentials (e.j.ps) were used as a measure of ATP release and continuous amperometry was used to measure NA release. 2. Varying the extracellular Ca2+ concentration similarly affected the amplitudes of e.j.ps and NA-induced oxidation currents evoked by trains of ten stimuli at 1 Hz. 3. The N-type Ca2+ blocker, omega-conotoxin GVIA (omega-CTX GVIA, 0.1 microM) reduced the amplitudes of both e.j.ps (evoked by trains of ten stimuli at 1 Hz) and NA-induced oxidation currents (evoked by trains of ten stimuli at 1 Hz and 50 stimuli at 10 Hz) by about 90%. 4. The omega-CTX GVIA resistant e.j.ps and NA-induced oxidation currents evoked by trains of 50 stimuli at 10 Hz were abolished by the non-selective Ca2+ channel blocker, Cd2+ (0.1 mM), and were reduced by omega-conotoxin MVIIC (0.5 microM) and omega-agatoxin IVA (40 nM). 5. Nifedipine (10 microm) had no inhibitory effect on omega-CTX GVIA resistant e.j.ps and NA-induced oxidation currents. 6. Thus both varying Ca2+ concentration and applying Ca2+ channel blockers results in similar effects on NA and ATP release from postganglionic sympathetic nerves. These findings are consistent with the hypothesis that NA and ATP are co-released together from the sympathetic nerve terminals.
摘要
  1. 体外研究了钙离子(Ca2+)浓度和Ca2+通道阻滞剂对大鼠尾动脉节后交感神经去甲肾上腺素(NA)和5'-三磷酸腺苷(ATP)释放的影响。细胞内记录的兴奋性接头电位(e.j.ps)用作ATP释放的指标,连续安培法用于测量NA释放。2. 改变细胞外Ca2+浓度同样影响1 Hz下10次刺激串诱发的e.j.ps幅度和NA诱导的氧化电流。3. N型Ca2+阻滞剂ω-芋螺毒素GVIA(ω-CTX GVIA,0.1 μM)使1 Hz下10次刺激串诱发的e.j.ps幅度和1 Hz下10次刺激串以及10 Hz下50次刺激串诱发的NA诱导的氧化电流幅度降低约90%。4. 10 Hz下50次刺激串诱发的对ω-CTX GVIA耐药的e.j.ps和NA诱导的氧化电流被非选择性Ca2+通道阻滞剂Cd2+(0.1 mM)消除,并被ω-芋螺毒素MVIIC(0.5 μM)和ω-阿加毒素IVA(40 nM)降低。5. 硝苯地平(10 μM)对ω-CTX GVIA耐药的e.j.ps和NA诱导的氧化电流无抑制作用。6. 因此,改变Ca2+浓度和应用Ca2+通道阻滞剂对节后交感神经NA和ATP释放产生相似的影响。这些发现与NA和ATP从交感神经末梢共同释放的假说一致。

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