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
复制
发表时间:
1985
影响因子:
7.3
通讯作者:
J. McGrath
中科院分区:
文献类型:
--
作者:
N. Flavahan;T. L. Grant;J. Greig;J. McGrath
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.