Tavernier G, Damase-Michel C, Tran M A, Montastruc J L, Montastruc P
Laboratoire de pharmacologie médicale et clinique, INSERM U317, faculté de médecine, Toulouse.
Arch Mal Coeur Vaiss. 1992 Aug;85(8):1137-40.
The release of catecholamines and their co-neurotransmitter neuropeptide Y was investigated in conscious dogs with neurogenic arterial hypertension elicited by sinoaortic denervation. One month after denervation, an elevation of catecholamine levels (measured by HPLC) without elevation of neuropeptide Y levels in plasma (evaluated by RIA) has been found. This dissociation could be explained by a transient release of neuropeptide Y during the first weeks after surgery; a depletion of neuronal neuropeptide Y due to the permanent sympathetic stimulation; or an insufficient increase in sympathetic tone. To test these three hypotheses, we investigated the time courses of catecholamine and neuropeptide Y levels in arterial plasma during the first five weeks after sinoaortic denervation; and the responses to yohimbine (an alpha 2 antagonist which enhances transmitter release). Resting neuropeptide Y levels in plasma remained normal during the first five weeks after sinoaortic denervation. In normal dogs, a high dose of yohimbine (0.5 mg/kg i.v.) elevated both catecholamine (6-fold) and neuropeptide Y levels (1.5-fold), whereas a lower dose (0.05 mg/kg i.v.) induced a two fold elevation of catecholamine levels without changing neuropeptide Y concentrations. In sinoaortically denervated dogs, yohimbine elicited elevation of both catecholamines and neuropeptide Y whatever the dose used. Thus, neurogenic arterial hypertension in dogs seams to involve catecholamines but not neuropeptide Y. Moreover, the present work suggests that a high level of sympathetic stimulation is required for a co-release of catecholamines and neuropeptide Y.
我们研究了在通过去窦主动脉神经支配诱发神经源性动脉高血压的清醒犬中儿茶酚胺及其共同神经递质神经肽Y的释放情况。去神经支配一个月后，发现血浆中儿茶酚胺水平升高（通过高效液相色谱法测定），而神经肽Y水平未升高（通过放射免疫分析法评估）。这种分离现象可以用术后最初几周神经肽Y的短暂释放、由于永久性交感神经刺激导致神经元神经肽Y的耗竭或交感神经张力增加不足来解释。为了验证这三个假设，我们研究了去窦主动脉神经支配后前五个星期动脉血浆中儿茶酚胺和神经肽Y水平的时间进程，以及对育亨宾（一种增强递质释放的α2拮抗剂）的反应。去窦主动脉神经支配后的前五个星期，血浆中静息神经肽Y水平保持正常。在正常犬中，高剂量的育亨宾（0.5毫克/千克静脉注射）使儿茶酚胺水平升高6倍，神经肽Y水平升高1.5倍，而低剂量（0.05毫克/千克静脉注射）使儿茶酚胺水平升高两倍，而神经肽Y浓度不变。在去窦主动脉神经支配的犬中，无论使用何种剂量，育亨宾都会使儿茶酚胺和神经肽Y水平升高。因此，犬的神经源性动脉高血压似乎涉及儿茶酚胺，但不涉及神经肽Y。此外，目前的研究表明，儿茶酚胺和神经肽Y的共同释放需要高水平的交感神经刺激。
