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内源性精氨酸合成不足会耗尽一氧化氮合成所需的底物精氨酸,从而引发高血压。

Deficiency of endogenous arginine synthesis provokes hypertension by exhausting substrate arginine for nitric oxide synthesis.

作者信息

Wakabayashi Y, Yamada E, Yoshida T, Takahashi H

机构信息

Department of Biochemistry, Kyoto Prefectural University of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 1994 Dec 15;205(2):1391-8. doi: 10.1006/bbrc.1994.2820.

DOI:10.1006/bbrc.1994.2820
PMID:7802675
Abstract

Effect of deficiency in endogenous arginine synthesis was studied in connection with NO synthesis and blood pressure. Rats with massive resection of small intestine were fed an arginine-free diet (AF rats) for 24 days. Control rats were pair-fed an isonitrogenous and isocaloric arginine-replete diet. AF rats lost weight by a mean of 28 g whereas control rats kept original weight. Urinary excretion of nitrate and cGMP was reduced in AF rats by about 40% after the feeding. Blood pressure became elevated by 20-25 mmHg in AF rats after the feeding. The concentrations of arginine in muscle and plasma of AF rats were reduced to 17 and 39%, respectively, of control rats. AF rats may be a novel animal model for the in vivo study of NO.

摘要

研究了内源性精氨酸合成缺乏与一氧化氮合成及血压的关系。对小肠大部切除的大鼠给予无精氨酸饮食(AF大鼠)24天。对照大鼠给予等氮等热量的富含精氨酸饮食。AF大鼠体重平均减轻28克,而对照大鼠体重保持不变。喂养后,AF大鼠尿中硝酸盐和环鸟苷酸排泄减少约40%。喂养后AF大鼠血压升高20 - 25 mmHg。AF大鼠肌肉和血浆中精氨酸浓度分别降至对照大鼠的17%和39%。AF大鼠可能是用于一氧化氮体内研究的新型动物模型。

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Deficiency of endogenous arginine synthesis provokes hypertension by exhausting substrate arginine for nitric oxide synthesis.内源性精氨酸合成不足会耗尽一氧化氮合成所需的底物精氨酸,从而引发高血压。
Biochem Biophys Res Commun. 1994 Dec 15;205(2):1391-8. doi: 10.1006/bbrc.1994.2820.
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