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突触前多巴胺受体作为多巴胺诱导的神经源性血管收缩抑制的介质。

Presynaptic dopamine receptors as mediators of dopamine-induced inhibition of neurogenic vasoconstriction.

作者信息

Lokhandwala M F, Buckley J P

出版信息

Eur J Pharmacol. 1977 Oct 1;45(3):305-9. doi: 10.1016/0014-2999(77)90015-2.

Abstract

I.v. infusion of dopamine (10 microgram/kg/min) caused significant attenuation of renal vasoconstrictor responses to sympathetic nerve stimulation in pentobarbital-anesthetized dogs, whereas renal vasoconstrictor responses to exogenously administered norepinephrine were unaffected. Desipramine treatment significantly potentiated the inhibitory effect of dopamine on neurogenic vasoconstriction. Pretreatment with pimozide, a dopamine receptor blocking agent, prevented the inhibitory influence of dopamine on renal sympathetic nerve function. These results demonstrate that dopamine can inhibit neurogenic vasoconstriction by activating presynaptic dopamine receptors present on renal sympathetic nerves.

摘要

静脉输注多巴胺(10微克/千克/分钟)可显著减弱戊巴比妥麻醉犬肾血管对交感神经刺激的收缩反应,而对肾血管对外源性去甲肾上腺素的收缩反应无影响。地昔帕明治疗可显著增强多巴胺对神经源性血管收缩的抑制作用。用多巴胺受体阻断剂匹莫齐特预处理可防止多巴胺对肾交感神经功能的抑制作用。这些结果表明,多巴胺可通过激活肾交感神经上的突触前多巴胺受体来抑制神经源性血管收缩。

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