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[神经肽Y、交感神经系统、高血压与α-2肾上腺素能受体]

[Neuropeptide Y, orthosympathetic nervous system, hypertension and alpha-2 adrenergic receptors].

作者信息

Poncet M F, Tavernier G, Damase-Michel C, Tran M A, Berlan M, Montastruc J L, Montastruc P

机构信息

Laboratoire de pharmacologie médicale et clinique, INSERM U317, faculté de médecine, Toulouse.

出版信息

Arch Mal Coeur Vaiss. 1991 Aug;84(8):1239-41.

PMID:1659347
Abstract

Neuropeptide Y (NPY) is coreleased with noradrenaline (NA) from sympathetic nerve endings. In vitro data suggest that NPY is coreleased during high stimulation frequencies. The present study investigates plasma levels of catecholamines and neuropeptide Y (NPY) during changes in sympathetic nervous activity in conscious dogs. Increase in sympathetic tone: arterial hypertension elicited by sinoaortic denervation induced an increase (X 2) in plasma noradrenaline (NA) but no change in NPY levels. High (0.5 mg/kg i.v.) but not low (0.05 mg/kg i.v.) doses of yohimbine rose plasma NPY concentrations. Decrease in sympathetic tone: clonidine (10 micrograms/kg i.v.) but not beta-blocking agents (propranolol or atenolol: 1 mg/kg i.v.) reduced plasma NPY levels. These results show that NPY is correleased in vivo from sympathetic nerve endings during marked and rapid increases in sympathetic tone. They suggest a lack of relationship between NA and NPY release. Alpha 2-adrenoceptors are involved in the presynaptic control of NPY release from sympathetic tone. Finally, some antihypertensive drugs (clonidine but not beta-blocking agents) are able to decrease plasma NPY levels.

摘要

神经肽Y(NPY)与去甲肾上腺素(NA)从交感神经末梢共同释放。体外数据表明,NPY在高刺激频率下共同释放。本研究调查清醒犬交感神经活动变化期间血浆儿茶酚胺和神经肽Y(NPY)的水平。交感神经张力增加:窦主动脉去神经支配引起的动脉高血压导致血浆去甲肾上腺素(NA)增加(X 2),但NPY水平无变化。高剂量(静脉注射0.5mg/kg)而非低剂量(静脉注射0.05mg/kg)的育亨宾使血浆NPY浓度升高。交感神经张力降低:可乐定(静脉注射10μg/kg)而非β受体阻滞剂(普萘洛尔或阿替洛尔:静脉注射1mg/kg)降低血浆NPY水平。这些结果表明,在交感神经张力显著快速增加期间,NPY在体内从交感神经末梢共同释放。它们提示NA和NPY释放之间缺乏关联。α2肾上腺素受体参与交感神经张力对NPY释放的突触前控制。最后,一些抗高血压药物(可乐定而非β受体阻滞剂)能够降低血浆NPY水平。

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1
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Arch Mal Coeur Vaiss. 1991 Aug;84(8):1239-41.
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