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。据报道，利钠因子参与了钠滞留的调节，这被认为是导致高血压的原因之一。利钠因子通过抑制&lt；Na^&gt；-&lt；K^&gt；ATPase而促进肾脏钠的分泌，从而增加细胞内钠在动脉壁的存留量。因此，&lt；Na^&gt；-&lt；Ca^()&gt；交换反应引起的细胞内钙升高可能导致血管对升压物质的超敏反应。孕期可通过增加体液和钠滞留刺激利钠因子的分泌，从而可能导致妊娠毒血症。用Hamlyn法测定血中&lt；Na^&Gt；-&lt；K^&Gt；ATPase抑制物的活性，发现妊娠中毒症患者其活性明显高于正常妊娠者，且平均血压与其活性呈显著正相关。脐静脉的活性高于脐动脉的活性，表明胎盘中有该因子的产生。前列腺素(PG)和前列腺素(Pg)具有松弛血管的降压作用。因此，血管内皮细胞中PG和I_2&GT；产生的活性受损可能会增加血管对升压物质的敏感性。我们的实验结果表明，轻度中毒血症时，PG&lt；I_2&Gt；的生成比正常妊娠时激活得更多，而重度中毒血症时，其生成受到很大程度的限制，从而可能加重毒血症。

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.