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血浆多巴胺对犬肾血流量的调节作用。

Plasma dopamine in regulation of canine renal blood flow.

作者信息

Kapusta D R, Robie N W

机构信息

Department of Pharmacology and Experimental Therapeutics, Louisiana State University Medical Center, New Orleans 70119.

出版信息

Am J Physiol. 1988 Sep;255(3 Pt 2):R379-87. doi: 10.1152/ajpregu.1988.255.3.R379.

Abstract

Studies were performed in pentobarbital-anesthetized dogs to determine whether circulating plasma dopamine (DA) is involved in renal blood flow (RBF) regulation. During graded reductions in renal perfusion pressure (RPP), total renal venous (RV) DA content significantly increased at RPPs below the autoregulatory range. The RBF response to decrements in RPP was also examined during control, infusion of DA (1.2 micrograms.kg(-1).min(-1)ia), and after DA receptor blockade by SCH 23390 (30 micrograms/kg iv). During DA infusion, autoregulation was still evident over the same RPPs, although at higher flow rates. At pressures below the autoregulatory range, RBF decreased linearly and the autoregulatory curve merged with control at 50 mmHg. After SCH 23390, autoregulation ceased at a higher RPP than during control, and RBF was significantly less than control rates at pressures of 80 mmHg and below. To elucidate reasons for this latter response, reductions in RPP were repeated before and after administration of both prazosin (0.1 mg/kg iv) and SCH 23390. The results indicated that RBF rates were not different from control at any RPP. Further, prazosin alone did not alter renal autoregulation but significantly increased RBF at RPP below the autoregulatory range. Thus these results indicate that dopamine does not participate in RBF control at pressures above the inflection point for the lowest limit of RBF autoregulation but may be released at lower RPP to act as a vasodilator agent to oppose alpha-adrenoceptor-mediated reductions in RBF. Moreover, tonic DA receptor activation may influence the setting of the lower limit of canine RBF autoregulation.

摘要

在戊巴比妥麻醉的犬身上进行了研究,以确定循环血浆多巴胺(DA)是否参与肾血流量(RBF)的调节。在肾灌注压(RPP)逐步降低的过程中,当RPP低于自身调节范围时,肾静脉(RV)总DA含量显著增加。在对照、输注DA(1.2微克·千克⁻¹·分钟⁻¹,静脉注射)以及用SCH 23390(30微克/千克,静脉注射)阻断DA受体后,还研究了RBF对RPP降低的反应。在输注DA期间,尽管流速较高,但在相同的RPP范围内仍能明显观察到自身调节。在低于自身调节范围的压力下,RBF呈线性下降,且自身调节曲线在50 mmHg时与对照曲线合并。注射SCH 23390后,自身调节在比对照更高的RPP时停止,并且在80 mmHg及以下的压力下,RBF显著低于对照速率。为了阐明后一种反应的原因,在给予哌唑嗪(0.1毫克/千克,静脉注射)和SCH 23390之前和之后重复降低RPP。结果表明,在任何RPP下,RBF速率与对照无差异。此外,单独使用哌唑嗪不会改变肾自身调节,但在低于自身调节范围的RPP时显著增加RBF。因此,这些结果表明,多巴胺在高于RBF自身调节下限拐点的压力下不参与RBF控制,但可能在较低的RPP时释放,作为一种血管舒张剂来对抗α-肾上腺素能受体介导的RBF降低。此外,持续性DA受体激活可能会影响犬RBF自身调节下限的设定。

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