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阿扑吗啡和培高利特对原位自体灌流大鼠肾和肠系膜上血管床去甲肾上腺素能神经传递的抑制作用。

Inhibition of noradrenergic neurotransmission by apomorphine and pergolide in the in situ autoperfused rat renal and superior mesenteric vascular beds.

作者信息

Dupont A G, Lefebvre R A, Bogaert M G

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1986 Jul;333(3):229-34. doi: 10.1007/BF00512934.

Abstract

In vitro studies have provided evidence that presynaptic dopamine receptors are present in the rat renal and superior mesenteric vascular beds. To confirm this in vivo, the effects of locally administered apomorphine and pergolide were studied in the in situ autoperfused renal and superior mesenteric vascular beds. Local infusion of apomorphine (1 microgram X kg-1 X min-1 for 5 min) or pergolide (1 microgram X kg-1 X min-1 for 5 min) into either the renal or the superior mesenteric artery had no effect on perfusion pressure per se. In the renal vascular bed, the pressure response to electrical stimulation (4 Hz, 1 ms, supramaximal voltage) was reduced to 49.8 +/- 4.8% by apomorphine and to 54.8 +/- 2.7% by pergolide; in the mesenteric vascular bed, apomorphine reduced the pressure response to electrical stimulation (4 Hz, 1 ms, supramaximal voltage) to 53.8 +/- 2.9, pergolide to 52.0 +/- 1.8%. Increases of perfusion pressure in the renal and in the mesenteric vascular bed induced by locally administered noradrenaline were not modified by apomorphine or pergolide. In both vascular beds, the inhibition of the stimulation-evoked pressure responses by apomorphine or pergolide was completely antagonized by local administration of the dopamine receptor antagonist haloperidol in a dose (1 microgram X kg-1) which did not influence the inhibitory effect of the alpha 2-adrenoceptor agonist UK-14,304; the alpha 2-adrenoceptor antagonist rauwolscine, in a dose (100 micrograms X kg-1) which completely antagonized the inhibitory effect of UK-14,304, did not antagonize the inhibitory effects of apomorphine and pergolide.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

体外研究已提供证据表明,大鼠肾和肠系膜上血管床中存在突触前多巴胺受体。为在体内证实这一点,对原位自灌注肾和肠系膜上血管床中局部给予阿扑吗啡和培高利特的作用进行了研究。向肾动脉或肠系膜上动脉局部输注阿扑吗啡(1微克·千克⁻¹·分钟⁻¹,持续5分钟)或培高利特(1微克·千克⁻¹·分钟⁻¹,持续5分钟)本身对灌注压无影响。在肾血管床中,阿扑吗啡使对电刺激(4赫兹,1毫秒,超最大电压)的压力反应降低至49.8±4.8%,培高利特使之降低至54.8±2.7%;在肠系膜血管床中,阿扑吗啡使对电刺激(4赫兹,1毫秒,超最大电压)的压力反应降低至53.8±2.9%,培高利特使之降低至52.0±1.8%。局部给予去甲肾上腺素引起的肾和肠系膜血管床灌注压升高未被阿扑吗啡或培高利特改变。在两个血管床中,阿扑吗啡或培高利特对刺激诱发压力反应的抑制作用可被局部给予多巴胺受体拮抗剂氟哌啶醇(剂量为1微克·千克⁻¹)完全拮抗,该剂量不影响α₂-肾上腺素能受体激动剂UK-14,304的抑制作用;α₂-肾上腺素能受体拮抗剂萝芙木碱(剂量为100微克·千克⁻¹)可完全拮抗UK-14,304的抑制作用,但不拮抗阿扑吗啡和培高利特的抑制作用。(摘要截于250字)

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