Cheav S L, Chahine R, Prigent A F
Laboratoire de Pharmacodynamie, Unité de Formation et de Recherche de Pharmacie, Tours, France.
Arzneimittelforschung. 1992 Nov;42(11):1288-91.
In the present investigation, the solvent glycerol acetonide (GA, CAS 100-79-8) was added (110 mg/min) to the Tyrode buffer perfusing an isolated rabbit heart preloaded with 14C-noradrenaline (NA). GA inhibits the neuronal uptake of NA but stimulates its spontaneous release. The latter effect was not ascribed to the stimulation of NA biosynthesis or to an inhibition of its catabolism. Moreover GA inhibits the evoked-release of the transmitter by tyramine and dimethyl phenyl piperazinium (DMPP). By stimulating the spontaneous release of NA, GA may induce both a depletion of myocardial stores and an important increase of the transmitter, inhibiting thereby the evoked-release by a negative feed-back mechanism on presynaptic alpha 2 adrenoceptors. Hence, the impact of GA on some steps of the cardiac adrenergic transmission may provide an adequate explanation for its observed hypotensive effect.
在本研究中，将溶剂甘油缩丙酮（GA，化学物质登记号100 - 79 - 8）以110毫克/分钟的速度加入到灌注预先加载了14C - 去甲肾上腺素（NA）的离体兔心脏的台氏缓冲液中。GA抑制NA的神经元摄取，但刺激其自发释放。后一种效应并非归因于对NA生物合成的刺激或对其分解代谢的抑制。此外，GA抑制酪胺和二甲基苯基哌嗪（DMPP）诱发的递质释放。通过刺激NA的自发释放，GA可能导致心肌储存的耗竭以及递质的显著增加，从而通过对突触前α2肾上腺素能受体的负反馈机制抑制诱发释放。因此，GA对心脏肾上腺素能传递某些步骤的影响可能为其观察到的降压作用提供充分的解释。
