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原发性高血压中盐诱导及自发性的磷脂酶C活性亢进

Salt-induced and spontaneous hyperactivity of phospholipase C in primary hypertension.

作者信息

Marche P, Limon I, Koutouzov S, Knorr A, Meyer P

机构信息

Department of Pharmacology, INSERM U 7, CNRS UA 318, Necker Hospital, Paris, France.

出版信息

J Hypertens Suppl. 1989 Dec;7(6):S120-1. doi: 10.1097/00004872-198900076-00056.

DOI:10.1097/00004872-198900076-00056
PMID:2632692
Abstract

Previous studies from our laboratory have shown that platelets from both spontaneously hypertensive rats and essential hypertensive patients exhibited an increased thrombin-triggered phospholipase C activity compared with normotensive subjects. In order to determine the relationship between phospholipase C and hypertension we investigated this enzymatic activity in Dahl salt-resistant (Dahl R/Jr) and salt-sensitive (Dahl S/Jr) rats fed either a low- or a high-NaCl diet, and in DOCA-NaCl hypertensive rats. Phospholipase C activity was increased in the Dahl S/Jr rats fed a high-NaCl diet compared to a low-NaCl diet. This difference was not observed in the Dahl R/Jr rats, irrespective of diet. Likewise, phospholipase C activity was similar in the DOCA-NaCl hypertensive rats compared with their controls. Our results indicate that the increased platelet phospholipase C activity was not a consequence of either the blood pressure elevation or the high NaCl intake and was probably of genetic origin. While the increased phospholipase C activity was not correlated with blood pressure, the enhanced enzymatic activity in Dahl S/Jr hypertensive rats may be involved in the elevation of blood pressure and may be NaCl-regulated.

摘要

我们实验室之前的研究表明,与血压正常的受试者相比,自发性高血压大鼠和原发性高血压患者的血小板在凝血酶触发下的磷脂酶C活性均有所增加。为了确定磷脂酶C与高血压之间的关系,我们研究了喂食低钠或高钠饮食的 Dahl 盐抵抗(Dahl R/Jr)和盐敏感(Dahl S/Jr)大鼠以及去氧皮质酮-盐(DOCA-NaCl)高血压大鼠的这种酶活性。与喂食低钠饮食的 Dahl S/Jr 大鼠相比,喂食高钠饮食的 Dahl S/Jr 大鼠的磷脂酶C活性增加。无论饮食如何,在 Dahl R/Jr 大鼠中均未观察到这种差异。同样,DOCA-NaCl 高血压大鼠与其对照组相比,磷脂酶C活性相似。我们的结果表明,血小板磷脂酶C活性增加不是血压升高或高钠摄入的结果,可能起源于遗传。虽然磷脂酶C活性增加与血压无关,但 Dahl S/Jr 高血压大鼠中增强的酶活性可能与血压升高有关,并且可能受氯化钠调节。

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