Literature DB >> 2802003

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

M S Paller1, G Gregorini, T F Ferris.   

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.

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Year:  1989        PMID: 2802003     DOI: 10.1152/ajpregu.1989.257.4.R866

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  6 in total

1.  The impact of maternal protein restriction during rat pregnancy upon renal expression of angiotensin receptors and vasopressin-related aquaporins.

Authors:  Ruth Cornock; Simon C Langley-Evans; Ali Mobasheri; Sarah McMullen
Journal:  Reprod Biol Endocrinol       Date:  2010-08-31       Impact factor: 5.211

2.  Mechanisms of vasodilatation in pregnancy: studies of the role of prostaglandins and nitric-oxide in changes of vascular reactivity in the in situ blood perfused mesentery of pregnant rats.

Authors:  Z M Chu; L J Beilin
Journal:  Br J Pharmacol       Date:  1993-06       Impact factor: 8.739

3.  Mesenteric arterial function in the rat in pregnancy: role of sympathetic and sensory-motor perivascular nerves, endothelium, smooth muscle, nitric oxide and prostaglandins.

Authors:  V Ralevic; G Burnstock
Journal:  Br J Pharmacol       Date:  1996-04       Impact factor: 8.739

4.  The role of nitric oxide in the altered vascular reactivity of pregnancy in the rat.

Authors:  L Nathan; J Cuevas; G Chaudhuri
Journal:  Br J Pharmacol       Date:  1995-03       Impact factor: 8.739

Review 5.  The Role of Placental Hormones in Mediating Maternal Adaptations to Support Pregnancy and Lactation.

Authors:  Tina Napso; Hannah E J Yong; Jorge Lopez-Tello; Amanda N Sferruzzi-Perri
Journal:  Front Physiol       Date:  2018-08-17       Impact factor: 4.566

Review 6.  Hormones and hemodynamics in pregnancy.

Authors:  Oleksandra Tkachenko; Dmitry Shchekochikhin; Robert W Schrier
Journal:  Int J Endocrinol Metab       Date:  2014-04-01
  6 in total

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