人类离体阻力动脉的神经诱发反应由α1和α2肾上腺素能受体介导。

Neurally evoked responses of human isolated resistance arteries are mediated by both alpha 1- and alpha 2-adrenoceptors.

作者信息

Parkinson N A, Thom S M, Hughes A D, Sever P S, Mulvany M J, Nielsen H

机构信息

Department of Clinical Pharmacology, St. Mary's Hospital Medical School, London.

出版信息

Br J Pharmacol. 1992 Jul;106(3):568-73. doi: 10.1111/j.1476-5381.1992.tb14376.x.

DOI:10.1111/j.1476-5381.1992.tb14376.x

PMID:1324074

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1907566/

Abstract

Human subcutaneous resistance arteries (internal diameter 113-626 microns) were mounted in an isometric myograph. Electrical field stimulation was applied either continuously in the form of a frequency-response curve or intermittently at 16 Hz. The magnitude of the maximum contraction induced by continuous stimulation expressed as a percentage of the response to a supramaximal concentration of noradrenaline (10 microM) was highly variable but unrelated to vessel calibre. Contractile responses to both continuous and intermittent stimulation were abolished by 1 microM tetrodotoxin. 2. Prazosin (100 nM and 1 microM, alpha 1-adrenoceptor antagonist) inhibited responses to continuous stimulation over a range of frequencies (2-8 Hz). The response to continuous stimulation at 8 Hz was inhibited by 78 +/- 6% by 1 microM prazosin. Rauwolscine (100 nM, alpha 2-adrenoceptor antagonist) had a smaller effect on contractions induced by continuous stimulation. Rauwolscine inhibited the response at 8 Hz by 36 +/- 6%. Rauwolscine at a higher concentration (1 microM) caused further inhibition of the response to continuous stimulation. Prazosin and rauwolscine in combination almost completely inhibited the response to continuous stimulation at concentrations of 1 microM. 3. Prazosin and rauwolscine inhibited responses to intermittent stimulation in a concentration-dependent manner. The IC50 for this action of prazosin was 3.7 +/- 1.6 nM and the maximum inhibition induced by 100 nM prazosin was 78 +/- 6%. The IC50 of rauwolscine was 12.0 +/- 1.3 nM and 100 nM rauwolscine caused a 86 +/- 7% reduction in the response to intermittent stimulation.Prazosin and rauwolscine in combination (each at 100 nM) caused marked inhibition of the response to intermittent stimulation leaving only 7.0 +/- 2.6% of the response.4. These data suggest that neurally released noradrenaline evokes contractions of human resistance arteries by activation of both alpha 1,- and alpha 2-adrenoceptors postjunctionally.

摘要

将人类皮下阻力动脉（内径113 - 626微米）安装在等长肌张力描记仪中。以频率响应曲线的形式持续施加电场刺激，或以16赫兹的频率间歇施加。持续刺激诱导的最大收缩幅度以对去甲肾上腺素（10微摩尔）超最大浓度反应的百分比表示，其变化很大，但与血管口径无关。1微摩尔的河豚毒素可消除对持续和间歇刺激的收缩反应。2. 哌唑嗪（100纳摩尔和1微摩尔，α1肾上腺素能受体拮抗剂）在一系列频率（2 - 8赫兹）范围内抑制对持续刺激的反应。1微摩尔哌唑嗪使8赫兹时对持续刺激的反应抑制了78±6%。育亨宾（100纳摩尔，α2肾上腺素能受体拮抗剂）对持续刺激诱导的收缩作用较小。育亨宾使8赫兹时的反应抑制了36±6%。更高浓度（1微摩尔）的育亨宾进一步抑制对持续刺激的反应。1微摩尔浓度的哌唑嗪和育亨宾联合使用几乎完全抑制对持续刺激的反应。3.哌唑嗪和育亨宾以浓度依赖性方式抑制对间歇刺激的反应。哌唑嗪此作用的半数抑制浓度（IC50）为3.7±1.6纳摩尔，100纳摩尔哌唑嗪诱导的最大抑制为78±6%。育亨宾的IC50为12.0±1.3纳摩尔，100纳摩尔育亨宾使对间歇刺激的反应降低86±7%。哌唑嗪和育亨宾联合使用（各100纳摩尔）显著抑制对间歇刺激的反应，仅留下7.0±2.6%的反应。4. 这些数据表明，神经释放的去甲肾上腺素通过激活节后α1和α2肾上腺素能受体引起人类阻力动脉收缩。