Day M D, Hall J M
Arch Int Pharmacodyn Ther. 1975 Jan;213(1):88-96.
Pressor responses to angiotensin II in the pithed rat were unaffected or slightly increased by procedures such as reserpine pretreatment, alpha and beta adrenoceptor blocking agents or bethanidine which inhibit the sympathetic system. Disulfiram-induced inhibition of angiotensin II pressor responses was unaffected by pretreatment with either alpha-adrenoceptor blockers or bethanidine. Pretreatment with disulfiram prevented infusions of angiotensin II from increasing the responses to spinal sympathetic outflow stimulation. After inhibition of pressor responses to angiotensin II by disulfiram the responses were restored by infusions of noradrenaline, or alpha-methyldopa. The restored responses, unlike control responses, were inhibited by phentolamine. The results suggest that angiotensin II facilitates neuronal release of noradrenaline and that this effect is revealed most clearly when post-synaptic angiotensin II receptors are blocked.
在脊髓横断的大鼠中,诸如利血平预处理、α和β肾上腺素能受体阻断剂或抑制交感神经系统的苄乙胍等处理,对血管紧张素II的升压反应没有影响或使其略有增加。双硫仑诱导的对血管紧张素II升压反应的抑制不受α-肾上腺素能受体阻断剂或苄乙胍预处理的影响。双硫仑预处理可防止输注血管紧张素II增加对脊髓交感神经传出刺激的反应。在双硫仑抑制血管紧张素II的升压反应后,输注去甲肾上腺素或α-甲基多巴可恢复该反应。与对照反应不同,恢复后的反应可被酚妥拉明抑制。结果表明,血管紧张素II促进去甲肾上腺素的神经元释放,并且当突触后血管紧张素II受体被阻断时,这种作用最为明显。