García A G, Sánchez-García P
Br J Pharmacol. 1975 Feb;53(2):247-55. doi: 10.1111/j.1476-5381.1975.tb07356.x.
1 The effects of cocaine and sodium on bretylium uptake into sympathetic nerve terminals were investigated in the reserpine-treated guinea-pig left atrium. The ability of bretylium pretreatment to increase the retention of noradrenaline was used as an index of bretylium uptake. Such increased retention has been assessed both by direct measurement and by the ability of tyramine to produce an inotropic response. 2 The restoration of the response to tyramine after incubation with noradrenaline was abolished when the atrium was pretreated with bretylium in the presence of cocaine. When bretylium was added before cocaine, or when alpha-methyl-noradrenaline (not a substrate for monoamine oxidase) was used for incubation, the responses to tyramine were restored in the normal way. 3 Bretylium greatly enhanced the retention of [3-H]-noradrenaline; when bretylium was added in the presence of cocaine, [3-H]-noradrenaline retention was severely impaired. 4 Pretreatment with bretylium in a low-sodium (25 mM) or sodium-free medium significantly decreased the retention of [3-H]-noradrenaline, as compared with the control. 5 Potassium deprivation did not modify the enhanced retention of [3-H]-noradrenaline induced by bretylium pretreatment. 6 Bretylium was released from the nerve terminals by exposure of the preparation to a sodium-free medium or to a solution containing calcium 50 mM, leading to a considerable decrease in [3-H]-noradrenaline retention. 7 The results are consistent with the view that both cocaine and sodium deprivation block the uptake of bretylium by the adrenergic nerve terminals, and that bretylium is probably taken up by a mechanism similar to or identical with the uptake system for noradrenaline and other amines.
1 在利血平处理过的豚鼠左心房中，研究了可卡因和钠对溴苄铵摄取到交感神经末梢的影响。溴苄铵预处理增加去甲肾上腺素潴留的能力被用作溴苄铵摄取的指标。这种增加的潴留已通过直接测量以及酪胺产生变力反应的能力进行评估。2 当心房在可卡因存在下用溴苄铵预处理时，与去甲肾上腺素孵育后对酪胺反应的恢复被消除。当在可卡因之前加入溴苄铵，或者当使用α-甲基去甲肾上腺素（不是单胺氧化酶的底物）进行孵育时，对酪胺的反应以正常方式恢复。3 溴苄铵极大地增强了[3-H]-去甲肾上腺素的潴留；当在可卡因存在下加入溴苄铵时，[3-H]-去甲肾上腺素的潴留严重受损。4 与对照相比，在低钠（25 mM）或无钠培养基中用溴苄铵预处理显著降低了[3-H]-去甲肾上腺素的潴留。5 钾缺乏并未改变溴苄铵预处理诱导的[3-H]-去甲肾上腺素潴留增强。6 通过将制剂暴露于无钠培养基或含有50 mM钙的溶液中，溴苄铵从神经末梢释放出来，导致[3-H]-去甲肾上腺素潴留显著降低。7 结果与以下观点一致，即可卡因和钠缺乏均阻断肾上腺素能神经末梢对溴苄铵的摄取，并且溴苄铵可能通过与去甲肾上腺素和其他胺类摄取系统相似或相同的机制被摄取。
