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

近年来，血管对升压物质的超敏反应作为妊娠毒血症的发病机制引起了人们的关注。钠尿因子参与钠潴留的调节，钠潴留被认为是导致原发性高血压的致病因素之一。利钠因子通过抑制<Na^+> - <K^+> ATP酶而刺激肾脏的钠分泌，另一方面，通过抑制<Na^+> - <K^+> ATP酶，可增加细胞内钠在动脉壁中的滞留。因此，由<Na^+> - <Ca^（++）>交换反应引起的细胞内Ca增加可诱导血管对升压物质的超敏反应。妊娠期可通过增加体液和钠潴留刺激利钠因子分泌，导致妊娠毒血症。用Hamlyn法测定血中Na^+-K^+ ATP酶抑制剂的活性，发现妊娠毒血症患者血中Na^+-K^+ ATP酶抑制剂的活性明显高于正常妊娠者，其活性与平均血压呈显著相关。脐静脉中的活性高于脐动脉中的活性，表明胎盘中产生了该因子。前列腺素（PG）<I_2>通过舒张血管来降低血压。因此<I_2>，血管内皮中PG产生的活性受损可能会增加血管对升压物质的敏感性。本实验结果表明，轻度毒血症时PG的生成<I_2>较正常妊娠时活跃，而重度毒血症时PG的生成受到很大程度的限制，使毒血症加重。

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.