硝苯地平对去脑大鼠中“嘌呤能”而非肾上腺素能神经介导的血管加压反应的选择性阻断作用。
Selective blockade by nifedipine of 'purinergic' rather than adrenergic nerve-mediated vasopressor responses in the pithed rat.
作者信息
Bulloch J M, McGrath J C
机构信息
Institute of Physiology, University of Glasgow.
出版信息
Br J Pharmacol. 1988 Nov;95(3):695-700. doi: 10.1111/j.1476-5381.1988.tb11695.x.
Abstract
- Nifedipine can attenuate pressor responses to sympathetic nerve stimulation both in the presence and in the absence of alpha-adrenoceptor blocking agents. 2. In the presence of alpha,beta-methylene ATP, nifedipine produces only a small attenuation of the vasopressor response. 3. Nifedipine attenuates the vasopressor response produced by intravenous bolus administration of alpha,beta-methylene ATP. 4. The results suggest that the purinergic component of the vasopressor response to stimulation of the sympathetic outflow in the rat is subject to blockade by nifedipine, whereas the alpha-adrenoceptor-mediated response to co-transmitter noradrenaline is relatively resistant.
摘要
- 硝苯地平在有或没有α-肾上腺素受体阻断剂存在的情况下，均可减弱对交感神经刺激的升压反应。2. 在存在α,β-亚甲基ATP的情况下，硝苯地平仅使血管升压反应略有减弱。3. 硝苯地平可减弱静脉推注α,β-亚甲基ATP所产生的血管升压反应。4. 结果表明，大鼠交感神经传出刺激引起的血管升压反应中的嘌呤能成分可被硝苯地平阻断，而对共递质去甲肾上腺素的α-肾上腺素受体介导反应则相对具有抗性。
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