Uteroplacental renin in regulation of blood pressure in the pregnant rabbit

Albertini, Rudolf von; Seino, Masahide; Scicli, A. G.; Carretero, Oscar A.

doi:10.1152/ajpheart.1980.239.2.h266

Cited by 14 publications

(9 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Indeed, the decrease in uterine blood flow produced in pregnant rabbits by All receptor blockade is reduced when the All receptor antagonist is given in combination with an ACE inhibitor (Albertini et al, 1980). In addition to effects on the cardiovascular system, the RAS has an important role in the expansion of maternal blood volume that occurs during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Comparison of angiotensin II type 1 receptor blockade and angiotensin‐converting enzyme inhibition in pregnant sheep during late gestation

Forhead

Whybrew

Hughes

et al. 1996

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of antagonism of the maternal renin-angiotensin system (RAS) with either an angiotensin II type 1-(ATI) specific receptor blocker (GR138950) or an angiotensin-converting enzyme (ACE) inhibitor (captopril) 9 The present study demonstrated that administration of either GR138950 or captopril to pregnant ewes effectively blocked the maternal RAS, and caused hypotension and a decrease in uterine blood flow. However, only captopril appeared to cross the placenta to influence directly the RAS of the sheep foetus. This suggests that the fall in foetal oxygenation observed after AT,-specific receptor blockade and ACE inhibition originates primarily from changes in the maternal and/or placental vasculature. Despite these changes, neither GR138950 nor captopril were detrimental to the outcome of pregnancy when foetal blood loss was kept to a minimum.

show abstract

Section: Discussionmentioning

confidence: 99%

Comparison of angiotensin II type 1 receptor blockade and angiotensin‐converting enzyme inhibition in pregnant sheep during late gestation

Forhead

Whybrew

Hughes

et al. 1996

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Elevated All may be required in pregnancy to overcome antagonism caused by increased synthesis of vasodilating prostaglandins. Saralasin, an angiotensin antagonist, significantly reduces arterial pressure in pregnant rabbits (15), and the decreased All responsiveness in pregnant women is reversed with indomethacin (16).…”

Section: Introductionmentioning

confidence: 99%

Effect of Captopril on Uterine Blood Flow and Prostaglandin E Synthesis in the Pregnant Rabbit

1983

View full text Add to dashboard Cite

A B S T R A C T Captopril, 5 mg/kg, administered to pregnant rabbits caused a reduction in mean arterial pressure (MAP) from 106±2 to 87±2 mmHg (P < 0.01) without change in cardiac output or renal blood flow.Uterine blood flow fell from 31.9±2.5 to 21.3±3.4 ml/ min (P < 0.01) as uterine vein prostaglandin E series level (PGE) decreased from 127±23 ng/ml to 26±8 ng/ml (P < 0.01). Saralasin also caused a reduction in MAP from 110±5 to 92±4.3 (P < 0.01), a reduction in uterine blood flow from 28.8±1.6 to 21.8±1.7 ml/ min (P < 0.01) as uterine vein PGE decreased from 121.3±14.4 to 63.5±14.2 ng/ml (P < 0.01). Plasma renin activity (PRA) was higher in the uterine vein, 11±3 ng/ml per h, than peripheral vein, 6±1.6 ng/ml per h, (P < 0.05), before Captopril and rose in the uterine vein to 90±19 ng/ml per h (P < 0.01) as peripheral vein PRA rose to 62±15 ng/ml per h (P <0.05) after Captopril. After saralasin uterine vein PRA rose from 4.6±1.5 to 14.8±6.3 ng/ml per h (P < 0.05) and peripheral vein PRA rose from 3.7±1 to 6.5±2.1 (P < 0.05).Reducing MAP with MgSO, from 98±4 to 70±2 (P < 0.01) caused a significant fall in cardiac output from 695±33 to 588±49 (P < 0.01) without change in renal or uterine blood flow. Uterine vein PGE concentration also did not change significantly following MgSO4; 80±22 ng/ml before and 60±27 ng/ml (NS) during the administration of MgSO4.Chronic administration of Captopril in doses of either 2.5 or 5.0 mg/kg per d from the 15th d of gestation caused an 86% fetal mortality at the lower and a 92% fetal mortality at the higher dose of the drug.These experiments point to the importance of uterine PGE synthesis in maintenance of uterine blood flow and fetal survival during pregnancy and suggest that uterine PGE synthesis is dependent upon angioAddress reprint requests to Dr. T.

show abstract

“…Previously, we have shown that chronic secondary renin-dependent hypertension (2 kidney-1 cellophane wrap hypertension; 2K-1W) in rabbit mothers does cause elevated arterial pressure in adult offspring (16,32). In this model, the elevation in maternal plasma renin activity (PRA) may also alter utero-placental blood flow, as the renin angiotensin system plays an important role in placental development (25,37,38) and in the local control of uteroplacental blood flow (2). Indeed, we have recently demonstrated that elevated maternal MAP and PRA, in a renindependent and a renin-independent model of hypertension differentially altered placental structural differentiation and disturbed the relationships between the placental renin-angiotensin system gene expression and placental structure (34).…”

mentioning

confidence: 99%

Chronic maternal hypertension characterized by renal dysfunction is associated with reduced placental blood flow during late gestation in rabbits

McArdle

Roberts

Maduwegedera

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Maternal hypertension associated with renal disease is a common pregnancy complication. Previously, we have shown in a rabbit model of mild hypertension that offspring from hypertensive mothers have increased blood pressure as adults. In human pregnancy, hypertension has been associated with decreased utero-placental blood flow. The aim of this study was to determine placental blood flow (PBF) in mild (2-kidney-1-wrapped; 2K-1W) and moderate (2-kidney-2-wrapped; 2K-2W) rabbit models of maternal hypertension. We hypothesized that PBF would be inversely related to the severity of the hypertension. PBF and renal blood flow (RBF) were measured using microspheres on day 28 of a 32-day gestation, in normotensive (sham), 2K-1W, and 2K-2W hypertensive groups. Mean arterial pressure (MAP, approximately 7 mmHg, P < 0.05) was increased, and RBF ( approximately 35%, P < 0.05) was reduced in the 2K-1W and 2K-2W (MAP approximately 20 mmHg, P < 0.01; RBF approximately 53%, P < 0.05) groups compared with the sham group. In the 2K-1W group, PBF fell by approximately 12% (P = 0.08) and fetal-to-placental weight ratio increased by approximately 12% (P < 0.01) compared with the sham group, reflecting an increase in the functional capacity of the placenta to deliver nutrients to the fetus. In the 2K-2W group, PBF decreased approximately 51% (P < 0.05) compared with the sham group, without changes in placental efficiency. Thus, in late gestation, placental blood flow was significantly reduced in the moderate hypertension group, without accompanying changes in fetal or placental weight or placental efficiency. In contrast, mild hypertension resulted in an increase in placental efficiency, without significant changes in placental blood flow. These findings suggest that mild and moderate hypertension may alter placental delivery of nutrients via differing mechanisms dependent upon the severity of the hypertension.

show abstract

Uteroplacental renin in regulation of blood pressure in the pregnant rabbit

Cited by 14 publications

References 0 publications

Comparison of angiotensin II type 1 receptor blockade and angiotensin‐converting enzyme inhibition in pregnant sheep during late gestation

Comparison of angiotensin II type 1 receptor blockade and angiotensin‐converting enzyme inhibition in pregnant sheep during late gestation

Effect of Captopril on Uterine Blood Flow and Prostaglandin E Synthesis in the Pregnant Rabbit

Chronic maternal hypertension characterized by renal dysfunction is associated with reduced placental blood flow during late gestation in rabbits

Contact Info

Product

Resources

About