Analysis of the α‐adrenoceptor‐mediated, and other, components in the sympathetic vasopressor responses of the pithed rat

Analysis of the α‐adrenoceptor‐mediated, and other, components in the sympathetic vasopressor responses of the pithed rat
复制标题

髓大鼠交感血管加压反应中α-肾上腺素受体介导的成分和其他成分的分析

DOI:
10.1111/j.1476-5381.1985.tb09458.x
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发表时间:
1985
影响因子:
7.3
通讯作者:
J. McGrath
J. McGrath
中科院分区:
医学2区
文献类型:
--
作者:
N. Flavahan;T. L. Grant;J. Greig;J. McGrath

文献摘要

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1通过分析“选择性”拮抗剂对去髓大鼠脊髓交感神经激活的血管加压反应的影响,确定交感-肾上腺刺激后激活的血管受体。2肾上腺刺激的净血管反应是α-肾上腺素受体介导的血管收缩和β-肾上腺素受体介导的血管抑制之间的平衡。部分α肾上腺素受体介导的反应是“哌唑嗪敏感”的(α1),其余反应被萝芙木碱消除(α2)。3.与刺激肾上腺一样,直接刺激交感神经引起的升压反应对哌唑嗪部分抵抗。萝芙木碱仅部分阻断哌唑嗪敏感组分。利血平预处理导致较小的反应比哌唑嗪加rauwolscine。因此,对α-肾上腺素受体拮抗剂耐药的反应可能部分由不同于目前定义的α-肾上腺素受体的肾上腺素受体介导。4 α,β-亚甲基ATP可降低α-肾上腺素受体阻滞剂或利血平预处理后神经介导的升压反应,但在无药物对照组中则无此作用。5结果表明,刺激肾上腺髓质可产生由α1和α2肾上腺素受体介导的成分总和组成的血管加压反应,与注射肾上腺素的作用相同。相反,对血管加压神经刺激的反应似乎基本上是由α1-肾上腺素受体介导的,α2-肾上腺素受体具有易化作用。α-肾上腺素受体阻滞后获得的进一步反应可能含有嘌呤能成分和另一种肾上腺素能成分,但不通过刺激α-肾上腺素受体介导。
1 The vascular receptors activated following sympatho‐adrenal stimulation were determined by analysing the effects of ‘selective’ antagonists on the vasopressor response to spinal sympathetic nerve activation in the pithed rat. 2 The net vascular response to adrenal stimulation was a balance between α‐adrenoceptor‐mediated vasoconstriction and β‐adrenoceptor‐mediated vasodepression. Part of the α‐adrenoceptor‐mediated response was ‘prazosin‐sensitive’ (α1) and the remainder was abolished by rauwolscine (α2). 3 As with adrenal stimulation, direct sympathetic nerve stimulation of the vasculature evoked pressor responses which were partly resistant to prazosin. Rauwolscine only partly blocked the prazosin‐sensitive component. Reserpine pretreatment led to smaller responses than prazosin plus rauwolscine. Thus, the response resistant to α‐adrenoceptor antagonists could be mediated, in part, by adrenoceptors distinct from α‐adrenoceptors, as currently defined. 4 α, β‐Methylene ATP reduced the nerve‐mediated pressor response after α‐adrenoceptor blockade or reserpine pretreatment but not in drug‐free controls. 5 The results suggest that stimulation of the adrenal medulla can produce a vasopressor response which consists of summating α1 and α2‐adrenoceptor‐mediated components, and is identical to the effect of injected adrenaline. In contrast, the response to vasopressor nerve stimulation appears to be essentially mediated by α1‐adrenoceptors, with a facilitatory influence from α2‐adrenoceptors. A further response obtained after α‐adrenoceptor blockade may contain a purinergic component and another which is adrenergic but not mediated by stimulation of α‐adrenoceptors.