摘要
为了解高血压病是否存在一氧化氮合酶（ＮＯＳ）遗传缺陷，采用同位素（３Ｈ－Ｌ精氨酸）法测定人血小板ＮＯＳ活性，观察高血压病（ＥＨ）患者（１９例）及有高血压病家族史的正常血压子女（ＦＨ＋，１３例）组的血小板在胶原（５μｇ／ｍｌ）激活下ＮＯＳ活性改变。结果：ＥＨ组和正常对照组（ＮＴ）、ＦＨ＋和无ＥＨ家族史的正常血压子女（ＦＨ－，１２例）组胶原激活的血小板ＮＯＳ活性分别为４．７６±２．０１比８．０９±２．３６ｐｍｏｌ·ｇ－１·ｍｉｎ－１、３．６４±２．０７比５．５１±２．１３ｐｍｏｌ·ｇ－１·ｍｉｎ－１（Ｐ＜０．０５）。表明ＥＨ组和ＦＨ＋组血小板ＮＯＳ活性均明显低于相应的对照组，提示ＥＨ有血小板ＮＯＳ活性缺陷，且与遗传因素有关，这可能是该病一种临床亚型，如进一步证实它是新的“遗传标记”，可为揭示ＥＨ相关基因及为早期预防合理治疗提供依据。
The collagen provocated platelet nitric oxide synthase (NOS) activity by the method of 3H labelled L arginine was compared between 19 essential hypertensives (EH) and 21 controls, and between 13 adolescents with their both parent hypertensives (FH +) and 12 adolescents without genetic hypertensive predisposition (FH -) as well. Results showed that the platelet NOS activity was lower significantly in EH group (4.76±2.01 vs 8 09±2 36 pmol·g -1 ·min -1 , P <0.001) and in FH + group (3 64±2 07 vs 5 51±2 13 pmol·g -1 ·min -1 , P <0.05) comparing with their control groups respectively. It suggests that the inherited defect of some anti hypertensive mechanisms like NO/NOS system may be implicated in the development of EH, which can be taken as a new “genetic marker” for detecting of specific clinic subtype. An useful data was thus presented of value in screening referred genes, for early prevention and rational remedy in essential hypertension.
出处
《中华内科杂志》
CAS
CSCD
北大核心
1997年第9期584-586,共3页
Chinese Journal of Internal Medicine
关键词
高血压
血小板
一氧化氮
连接酶类
Hypertension Blood platelets Nitric oxide Ligases
