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Study on the factors inducing hypersensitivity of the blood vessels to pressor substances in toxemia of pregnancy

妊娠毒血症血管对升压物质过敏的影响因素研究

基本信息

批准号：
60570769
负责人：
SATOH Kazuo
金额：
$ 1.34万
依托单位：
Saitama Medical Center, Saitama Medical College (1986)The University of Tokyo (1985)
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1985
资助国家：
日本
起止时间：
1985 至 1986
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-60570769/
关键词：
Toxemia of pregnancy <Na^+> - <K^+> ATPase Na利尿因子 PG【I_2】血圧

项目摘要

Attention has recently been focused on hypersensitivity of the blood vessels to pressor substances as pathogenesis of toxemia of pregnancy. Natriuretic factor is reported to be involved in regulation of Na retention which is suggested to be one of the causative factors leading to essential hypertension. Natriuretic factor has the stimulatory effect on Na secretion from the kidney by inhibition of <Na^+> - <K^+> ATPase, through which, on the other hand, the increased intracellular Na retention may be brought about in the arterial wall. Consequently, increased intracellular Ca resulting from <Na^+> - <Ca^(++)> exchange reaction may induce hypersensitivity of the blood vessels to pressor substances. Secretion of natriuretic factor may be stimulated during pregnancy through increased body fluid and Na retention, which might result in toxemia of preganacy. Measurement of the activity of <Na^+> - <K^+> ATPase inhibitor in the blood by Hamlyn's method revealed that its activity in toxemia of pregnancy was significantly higher than in normal pregnancy and significant correlation was observed between mean blood pressure and its activity. Higher activity in the umbilical vein than in the umbilical artery indicated production of the factor in the placenta.Prostaglandin(PG) <I_2> has the lowering effect on blood pressure by relaxation of the blood vessels. Impaired activity.of PG <I_2> production in the endothelium of the blood vessels, therefore, may increase sensitivity of the vessels to pressor substances. Our experimental results showed that production of PG <I_2> was activated in mild toxemia more than in normal pregnancy, whereas in severe one its production was restricted to great extent so that toxemia may be aggravated.

妊娠毒血症的发病机制主要是血管对加压物质的超敏反应。据报道，利钠因子参与钠潴留的调节，这被认为是导致原发性高血压的原因之一。利钠因子通过抑制<Na^+> - <K^+> atp酶刺激肾内Na分泌，另一方面可能导致动脉壁内细胞内Na潴留增加。因此，<Na^+> - <Ca^(++)>交换反应引起的细胞内Ca升高可能引起血管对加压物质的超敏反应。在妊娠期，尿钠因子的分泌可能通过增加体液和钠潴留而受到刺激，从而导致妊娠毒血症。Hamlyn's法测定<Na^+> - <K^+> atp酶抑制剂在妊娠毒血症中的活性明显高于正常妊娠，其活性与平均血压有显著相关性。脐静脉比脐动脉活性高表明胎盘中产生了该因子。前列腺素(PG) <I_2>通过血管舒张而降低血压。受损的活动。因此，血管内皮中PG <I_2>的产生可能增加血管对压力物质的敏感性。我们的实验结果表明，在轻度毒血症中，PG <I_2>的产生比正常妊娠更活跃，而在重度妊娠中，PG <I_2>的产生受到很大程度的限制，从而可能加重毒血症。