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脑多巴胺系统在自发性高血压大鼠高血压发生发展中的作用。

Role of brain dopamine systems in the development of hypertension in the spontaneously hypertensive rat.

作者信息

van den Buuse M, Linthorst A C, Versteeg D H, de Jong W

机构信息

Marion Merrell Dow Research Institute, Strasbourg Research Center, France.

出版信息

Clin Exp Hypertens A. 1991;13(5):653-9. doi: 10.3109/10641969109042068.

Abstract

We studied the role of central dopamine in the development of hypertension. Earlier work had shown that depletion of brain dopamine can inhibit the age-related rise in blood pressure in spontaneously hypertensive rats (SHR). In an open-field test, locomotor activity of Wistar-Kyoto controls was inhibited by haloperidol, apomorphine and sulpiride, but these drugs had less effect in SHR. The stimulation-evoked release of [3H]-dopamine from slices of the striatum of SHR was smaller than that from slices of WKY. The inhibition of the stimulation-evoked release of [3H]-dopamine by quinpirole was greater in SHR than in WKY. The results from the lesion experiments and from the behavioural activity studies would suggest an enhanced release of central dopamine in SHR, which might contribute to the development of hypertension in these animals. However, the in vitro release experiments (and subsequent in vivo microdialysis experiments) do not support such an enhanced release but rather showed decreased release of striatal dopamine in SHR.

摘要

我们研究了中枢多巴胺在高血压发生发展中的作用。早期研究表明,脑内多巴胺耗竭可抑制自发性高血压大鼠(SHR)与年龄相关的血压升高。在旷场试验中,氟哌啶醇、阿扑吗啡和舒必利可抑制Wistar-Kyoto对照大鼠的运动活性,但这些药物对SHR的作用较小。SHR纹状体切片中刺激诱发的[3H] - 多巴胺释放量小于WKY大鼠纹状体切片中的释放量。喹吡罗对SHR刺激诱发的[3H] - 多巴胺释放的抑制作用比对WKY大鼠的抑制作用更强。损伤实验和行为活动研究的结果表明,SHR中枢多巴胺释放增加,这可能导致这些动物发生高血压。然而,体外释放实验(以及随后的体内微透析实验)并不支持这种释放增加,反而显示SHR纹状体多巴胺释放减少。

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