妊娠ラットの体液分布及びangiotensin II, norepinephrineに対する昇圧反応性の検討

DOI

書誌事項

タイトル別名
  • BODY FLUID VOLUMES AND PRESSOR RESPONSE TO ANGIOTENSIN II AND NOREPINEPHRINE IN PREGNANT RATS

抄録

The aims of the present study were to examine the appropriateness of the rat as a model for human pregnancy in distribution of body fluid volumes and pressor response to vasoconstrictor substances. Body fluid volumes and the pressor response to angiotensin II (AII) and norepinephrine (NE) were determined in unanesthetized nonpregnant and pregnant rats, at 6-10 days gestation (early gestation) and 16-20 days gestation (late gestation). The distribution of body fluid volumes was measured by an isotope dilution method; plasma volume (PV), extracellular fluid volume (ECFV), and total body water (TBW) by 131I-radio-iodinated serum albumin, 35S-sodium sulfate, and tritiated water respectively. Late gestation rats had signficantly (p<0.01) increased PV and TBW but only slight increased ECFV when compared to nonpregnant rats, while the pregnant rats had elevated PRA values (p<0.01). The results are almost compatible with the data in human pregnancy. In early gestation, the pressor response to AII tended to decrease, while that to NE was found to be almost the same with that in nonpregnant rats. In late gestation, on the other hand, the pressor response to both AII and NE decreased significantly (p<0.05) compared with nonpregnant rats. The reduced AII pressor response in late gestation decreased further by the treatment with indomethacin (10mg per kg), while response to NE increased significantly (p<0.05) to the normal level in nonpregnant rats. The treatment did not alter the response to AII and NE in either nonpregnant or early gestation of rats. PRA was measured in other groups of unanesthetized pregnant and nonpregnant rats before and after the treatment with indomethacin. PRA values were significantly (p<0.05) elevated both in early and late gestation rats compared with nonpregnant rats before the treatment. The treatment did not change PRA values either in nonpregnant or early gestation rats, but increased them in late gestation rats. These results suggest that the mechanisms of reduced pressor response to AII and NE in late gestation rats might be different : the response to AII is mainly determined by the increased activity of the renin-angiotensin system, and that to NE might be related to increased vasodilator prostaglandins. The rat could serve as another animal model in investigating AII and NE refractoriness in pregnancy.

収録刊行物

詳細情報 詳細情報について

  • CRID
    1390001205331336448
  • NII論文ID
    130003689990
  • DOI
    10.2974/kmj1951.33.397
  • ISSN
    18836135
    00231908
  • データソース種別
    • JaLC
    • Crossref
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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