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假孕和怀孕大鼠的升压反应性:母体因素的作用

Pressor responsiveness in pseudopregnant and pregnant rats: role of maternal factors.

作者信息

Paller M S, Gregorini G, Ferris T F

机构信息

Department of Medicine, University of Minnesota, Minneapolis 55455.

出版信息

Am J Physiol. 1989 Oct;257(4 Pt 2):R866-71. doi: 10.1152/ajpregu.1989.257.4.R866.

Abstract

During pregnancy the pressor response to vasoconstrictor substances such as angiotensin II (ANG II) is diminished, and renal, uterine, and vascular prostaglandin (PG) production may increase. However, little is known about the factors that alter vascular reactivity or stimulate PG synthesis during pregnancy. To ascertain whether these factors are of maternal or fetal-placental origin, we studied vascular reactivity and urinary PGE excretion in pseudopregnant rats. Pseudopregnant rats had plasma progesterone and weight gain similar to that observed in pregnant rats. Urinary PG excretion in nonpregnant rats was approximately 70 ng/24 h and remained constant during a 12-day observation. In contrast, urinary PG excretion in both pregnant and in pseudopregnant rats rose to levels approximately twice control within 4-6 days. The pressor response to ANG II was diminished in pseudopregnant rats compared with nonpregnant rats. When the PG synthesis inhibitor meclofenamate was given there was no change in the pressor response to ANG II in nonpregnant animals, but in pseudopregnant animals meclofenamate produced a significant increase in the pressor response to ANG II. The pressor response to norepinephrine and arginine vasopressin (AVP) was not diminished in pseudopregnant animals, and meclofenamate did not increase the pressor response to these agents. Therefore, a developing fetus and placenta is not necessary for the decrease in pressor response to ANG II nor for the early increase in urinary PGE excretion. Like in pregnancy, the pressor response to ANG II was increased after meclofenamate in pseudopregnancy. Increased PG production may, therefore, be partly responsible for the decrease in pressor responsiveness to ANG II. However, pseudopregnancy, unlike pregnancy, did not affect pressor responsiveness to norepinephrine or AVP. Both maternal and fetal-placental factors seem required for the reduction in responsiveness to norepinephrine and AVP in pregnancy.

摘要

在怀孕期间,对血管收缩物质如血管紧张素II(ANG II)的升压反应减弱,肾脏、子宫和血管的前列腺素(PG)生成可能增加。然而,关于孕期改变血管反应性或刺激PG合成的因素知之甚少。为了确定这些因素是母体来源还是胎儿-胎盘来源,我们研究了假孕大鼠的血管反应性和尿PGE排泄。假孕大鼠的血浆孕酮和体重增加与妊娠大鼠相似。未孕大鼠的尿PG排泄量约为70 ng/24 h,在12天的观察期内保持恒定。相比之下,妊娠和假孕大鼠的尿PG排泄量在4 - 6天内升至约为对照水平两倍。与未孕大鼠相比,假孕大鼠对ANG II的升压反应减弱。给予PG合成抑制剂甲氯芬那酸后,未孕动物对ANG II的升压反应无变化,但在假孕动物中,甲氯芬那酸使对ANG II的升压反应显著增加。假孕动物对去甲肾上腺素和精氨酸加压素(AVP)的升压反应未减弱,甲氯芬那酸也未增加对这些药物的升压反应。因此,发育中的胎儿和胎盘对于ANG II升压反应的降低以及尿PGE排泄早期增加并非必需。与妊娠一样,假孕时甲氯芬那酸给药后对ANG II的升压反应增加。因此,PG生成增加可能部分导致了对ANG II升压反应性的降低。然而,与妊娠不同,假孕不影响对去甲肾上腺素或AVP的升压反应性。妊娠时对去甲肾上腺素和AVP反应性降低似乎需要母体和胎儿-胎盘因素共同作用。

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