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多巴胺在大鼠高血压发生发展中的病理生理作用。

Pathophysiological role of dopamine on the development of hypertension in rats.

作者信息

Yoshimura M, Kambara S, Okabayashi H, Ikegaiki I, Matsuzawa M, Suga K, Takahashi H, Ijichi H

机构信息

Second Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.

出版信息

Jpn Circ J. 1987 Oct;51(10):1226-31. doi: 10.1253/jcj.51.1226.

Abstract

The aim of the study is to investigate the pathophysiological role of dopamine (DA) in the development of hypertension in DOCA-salt hypertensive rats and spontaneously hypertensive rats (SHRs). The augmentation of dopaminergic activity by chronic administration of bromocriptine, a DA agonist, suppressed the increase of blood pressure in DOCA-salt hypertensive rats. In contrast, suppression of dopaminergic activity by chronic administration of carbidopa, an inhibitor of dopa decarboxylase, accelerated the development of hypertension in SHRs, and this acceleration was also increased by salt loading. Increased urinary excretion of norepinephrine (NE) by DOCA-salt treatment was suppressed by the treatment of bromocriptine. In contrast, administration of carbidopa and salt loading in SHRs resulted in an increase in renal NE content and in urinary NE and epinephrine (E) excretion and a decrease in urinary sodium excretion. These results suggest that dopaminergic activity participate in the development of hypertension and decreased dopaminergic activity accelerates the development of hypertension in hypertensive rats mainly through the enhancement of peripheral sympathetic nerve activity.

摘要

本研究的目的是探讨多巴胺(DA)在去氧皮质酮盐性高血压大鼠和自发性高血压大鼠(SHR)高血压发生发展中的病理生理作用。长期给予DA激动剂溴隐亭可增强多巴胺能活性,从而抑制去氧皮质酮盐性高血压大鼠的血压升高。相反,长期给予多巴脱羧酶抑制剂卡比多巴抑制多巴胺能活性,加速了SHR高血压的发展,且盐负荷会加剧这种加速作用。溴隐亭治疗可抑制去氧皮质酮盐处理导致的去甲肾上腺素(NE)尿排泄增加。相反,在SHR中给予卡比多巴和盐负荷会导致肾NE含量增加、尿NE和肾上腺素(E)排泄增加以及尿钠排泄减少。这些结果表明,多巴胺能活性参与高血压的发生发展,多巴胺能活性降低主要通过增强外周交感神经活性加速高血压大鼠高血压的发展。

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