Response of ovine uterine blood flow to angiotensin II: Effect on the fetus

Bruce, Samuel L.; Morishima, Hisayo O.; Petrie, Roy H.; Sakuma, Kaori; Daniel, Salha S.; Yeh, Shih-Ching

doi:10.1016/s0002-9378(15)33267-1

Cited by 10 publications

(4 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations are in agreement with previous studies with AT1 receptor blockers (Forhead et al, 1995) and ACE inhibitors (Lumbers et al, 1992). All receptors have been localised in the ovine uteroplacental circulation (Mackanjee et al, 1991), and All infusions have dose-dependent effects on blood flow and vascular resistance in the pregnant uterus (Bruce et al, 1981;Clarke et al, 1990). During All infusion in pregnant dogs, an increase in uterine vascular resistance and a decrease in uterine blood flow has been demonstrated in animals in which the uterine perfusion pressure was experimentally maintained at pretreatment values and was prevented from rising in response to the AII-induced increase in systemic blood pressure (Woods, 1993).…”

Section: Discussionsupporting

confidence: 92%

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: Discussionsupporting

confidence: 92%

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

“…Since probes measure flow through an isolated distal artery and 3H20 infusion measures total flow through uteroplacental and ovarian tissues, the temporal discrepancy between the two methods suggests that there may be a shift in the distribution of blood flow to various uteroplacental tissues after GR1 17289 treatmenit. Indeed, changes in the distribution of uterine blood flow to placental, endometrial and Inyometrial tissues have been observed in pregnant sheep following administration of captopril and All (Bruce, Morishima, Petrie, Sakuma, Daniel & Yeh, 1981;Rosenfeld & Gant, 1981;Lumbers et al 1992).…”

Section: Discussionmentioning

confidence: 99%

Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep

Forhead

Fowden²,

Silver³

et al. 1995

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYAn ATI-specific angiotensin II receptor antagonist (GRI 17289; 1 mg/kg I.v. bolus) was administered daily to ten chronically catheterized, normotensive ewes during late pregnancy (from 126 ± 1 days) until parturition (139 + 1 days); five control animals received an equivalent volume of vehicle solution. Following drug administration, mean maternal blood pressure decreased from 87 ± 1 mmHg to a minimum of 79 ± 1 mmHg at 0 5 h (P < 005; n = 10) and remained low for 4-6 h without any concomitant change in fetal blood pressure or maternal and fetal heart rates. In animals fitted with flow probes, uterine blood flow decreased from 443 ± 21 to 363 ± 27 ml/min at 0-5 h post-drug (P < 0 05; n = 6); this change was positively correlated with the reduction in maternal blood pressure. The mean decrements in uterine and umbilical blood flows measured by steady-state infusion of tritiated water were -611 ± 171 ml/min at 4-6 h (P < 0 05; n = 5) and -71 + 19 ml/min at 0-5-1 h (P < 0 05; n = 5), respectively. Significant reductions (P < 0-05; n = 10) in fetal arterial oxygen tension (-1 6 ± 0 4 mmHg), saturation (-6.6 ± 1 6 %) and content (-0.3 ± 0-1 4umol/ml) were evident at 0.5 h post-drug and were maintained for 6-12 h. Umbilical oxygen delivery decreased at 0 5-1 h following drug administration (P <001; n = 5), but was unaccompanied by any significant change in fetal oxygen consumption. Chronic decreases in daily fetal pH and blood oxygen content occurred in GRl 17289-treated ewes. There were no significant differences in gestational length or neonatal outcome between vehicle-and GRI 17289-treated groups of ewes with single fetuses.

show abstract

“…Specific and saturable angiotensin II binding has also been demonstrated in rat uterus (Lin & Goodfriend, 1970). Administered angiotensin II increases uterine blood flow in pregnant sheep (Bruce et al, 1981) and monkeys (Speroff et al, 1977); in the latter, this response is inhibited by indomethacin, a blocker of PG synthesis. Conversely, inhibition of angiotensin-converting enzyme reduces blood flow and PGE production in the uterus of pregnant rabbits (Ferris & Weir, 1983).…”

Section: Introductionmentioning

confidence: 99%

Evidence for a role for a uterine renin-angiotensin system in decidualization in rats

Squires¹,

Kennedy²

1992

Reproduction

View full text Add to dashboard Cite

Experiments were performed in vivo and in vitro to determine the effects of enalaprilat, a specific inhibitor of angiotensin-converting enzyme, on various aspects of the decidual cell reaction in rats. Ovariectomized, adult female rats were sensitized for the decidual cell reaction with steroid treatments. For in vivo experiments, intrauterine infusions of enalaprilat alone, and in combination with angiotensin II and prostaglandin E2 (PGE2), were initiated on the day of uterine sensitivity. Enalaprilat inhibited the increases in uterine PG concentrations, endometrial vascular permeability, alkaline phosphatase activity and uterine weight that occurred sequentially following infusion of vehicle. Concurrent infusion of angiotensin II did not reverse any of these inhibitory effects; PGE2 infusion partially, but not completely, reversed the inhibition of increase in uterine weight, although it did not alter the inhibition of endometrial vascular permeability. For in vitro experiments, endometrial stromal cells were obtained from uteri on the day of sensitivity and cultured for up to 3 days in the presence of enalaprilat and angiotensin II. Enalaprilat inhibited in a dose-dependent manner the increases in stromal cell alkaline phosphatase activity and media PGE concentration that occurred in the control cultures; these effects were fully reversed by concurrent treatment with angiotensin II. The inhibition of stromal alkaline phosphatase activity was also reversed by PGE2; conversely, the ability of angiotensin II to reverse the effect of enalaprilat was lost in the presence of indomethacin. These studies provide evidence of a requirement for angiotensin II during the decidual cell reaction in rats and suggest that it acts, at least in part, through a PG-dependent mechanism.

show abstract

Response of ovine uterine blood flow to angiotensin II: Effect on the fetus

Cited by 10 publications

References 3 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

Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep

Evidence for a role for a uterine renin-angiotensin system in decidualization in rats

Contact Info

Product

Resources

About