Angiotensin-converting enzyme activity and contractile effects of angiotensin I and II in human uteroplacental arteries

Svane, Danny; Kahr, Ole; Hansen, Vibeke Brogaard; Holm-Nielsen, P; Forman, Axel

doi:10.1016/0002-9378(95)90032-2

Cited by 26 publications

(10 citation statements)

References 30 publications

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“…Increased kininase activity could reduce the amount of peptide in the vicinity of the receptor and, consequently, contribute to a lesser final biological response. During normal pregnancy, local ACE activity has been reported in human intramyometrial arteries and placental membranes 35,36 . In the present study, we have shown that ACE inhibition by captopril potentiated BK vasodilator responses and abolished the differences between pregnant and non‐pregnant SHR.…”

Section: Discussionsupporting

confidence: 69%

Captopril Reverses the Reduced Vasodilator Response to Bradykinin in Hypertensive Pregnant Rats

Resende

Pimentel

Moura

2004

Clin Exp Pharma Physio

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1. Pregnancy in rats is characterized by a reduction in arterial pressure that is associated with a decreased response to vasoconstrictors. However, the responses to vasodilators in isolated vessels remain controversial and are not well established in hypertensive pregnant rats. 2. In the present study, we investigated the effect of pregnancy on the bradykinin (BK)-induced vasodilator responses of the isolated mesenteric arterial bed (MAB) from Wistar normotensive and spontaneously hypertensive rats (SHR) and determined the role of nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF) and angiotensin-converting enzyme (ACE) in these responses. 3. Mean arterial pressure (MAP) in pregnant normotensive and pregnant hypertensive rats (93 +/- 1 and 122 +/- 2 mmHg, respectively) was lower than in non-pregnant controls (128 +/- 1 and 163 +/- 2 mmHg, respectively; P < 0.05). In MAB isolated from normotensive rats and precontracted with phenylephrine, the effects of bradykinin, acetylcholine (ACh) and nitroglycerine (NG) were not influenced by pregnancy. In contrast, the vasodilator responses to BK were significantly reduced in pregnant compared with non-pregnant SHR and seemed to be specific to BK. 4. The ACE inhibitor captopril potentiated BK vasodilator responses and abolished the differences between pregnant and non-pregnant SHR. Inhibition of nitric oxide (NO) synthase by N(G)-nitro-L-arginine methyl ester (l-NAME) significantly reduced the vasodilator effect of BK in all groups. In the presence of l-NAME plus high K+ solution (47 mmol/L), BK-induced vasodilation was completely blocked. The NO-dependent component of the responses seems to be more important in hypertensive rats and pregnancy does not modify this profile. 5. Our results suggest that increased ACE activity may be involved in the pregnancy associated reduction in vasodilator responses to BK in the MAB of hypertensive rats. Pregnancy does not modify the relative contribution of the EDHF and NO to the vasodilator effect of BK.

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Section: Discussionsupporting

confidence: 69%

Captopril Reverses the Reduced Vasodilator Response to Bradykinin in Hypertensive Pregnant Rats

Resende

Pimentel

Moura

2004

Clin Exp Pharma Physio

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“…Our finding of a higher proportion of AT 1 receptors in the first part of gestation probably reflects a higher content of maternal tissue in the early placentomes. Previous studies showed that Ang II stimulated angiogenesis [32] and regulated uteroplacental blood-flow [8][9][10]. Autoradiography showed very little 125 I-[Sar 1 -Ile 5 -Ile 8 ]-Ang II binding in either arteries or minor blood vessels in the bovine placenta.…”

Section: Discussionmentioning

confidence: 97%

“…The known effects of Ang II in the uteroplacental unit have mainly been associated with the AT 1 receptor. In humans and in ewes, Ang II is one of the factors that regulate the blood flow in the uteroplacental unit, and it thereby indirectly influences the fetal volume homeostasis and oxygenation [8][9][10]. Ang II also stimulates placental lactogen, pregnancy-specific ␤ 1 -glycoprotein, and estradiol secretion in human trophoblast cells via AT 1 receptors [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Autoradiographic Localization and Characterization of Angiotensin II Receptors in the Bovine Placenta and Fetal Membranes1

Schauser¹,

Nielsen²,

Winther³

et al. 1998

Biology of Reproduction

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Autoradiography and angiotensin (Ang) II receptor binding studies showed that all parts of the bovine placenta and fetal membranes contained high densities of Ang II receptors throughout gestation. The receptors were predominantly subtype 2 (AT2) receptors in the fetal and subtype 1 (AT1) receptors in the maternal compartment. In the allantoamnionic membrane, Ang II receptors were evenly distributed in the mesenchymal tissue, with the highest expression around the few arteries. In the intercotyledonary and cotyledonary allantochorionic membrane, AT2 receptors as well as the less-expressed AT1 receptors were located on mesenchymal cells, especially adjacent to the allantoic endoderm, trophoblast cell layer, and arteries. In the mesenchymal tissue of the placentome, Ang II receptors were mostly expressed at the main branches of the fetal villi of the cotyledons. In the maternal part of the placentome, mainly AT1 receptors but also low densities of AT2 receptors and non-AT1/non-AT2 Ang II binding sites were found close to the stalk and at the main branches of the maternal crypts. Autoradiography revealed no changes in the pattern of distribution of the Ang II receptors throughout gestation. It is suggested that Ang II has an effect on regulatory as well as growth processes in these tissues.

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“…The angiotensin converting enzyme is present in stem villous arteries, but shows low activity (Svane, Kahr, Hansen, Holm-Nielsen & Forman, 1995) and receptors for All are present in placental tissue and umbilical artery (Tence & Petit, 1989). All contracts small fetoplacental arteries, but modestly, and the contractions are transient and subject to tachyphylaxis Svane et al 1995). In the umbilical artery, All has no constrictor effect at all (White, 1989).…”

Section: Fetal Cardiac Outputmentioning

confidence: 99%

The control of blood flow to the placenta

Poston¹

1997

Experimental Physiology

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SUMMARYThe maintenance of adequate blood flow to the placenta is essential for the successful outcome of pregnancy. The placental vascular bed is often regarded as a low-resistance circulation in which blood flow is determined by the fetal cardiac output, but in pregnancies associated with growth retardation, and for reasons unknown, vascular resistance increases and blood flow is compromised. This review concentrates on recent advances in our understanding of the factors that may influence fetoplacental blood flow, with particular emphasis upon the circulation of the human placenta. The placenta has no neuronal input and vascular resistance is entirely determined by humoral and structural factors. In the absence of catecholamine sensitivity, constrictor prostanoids and endothelin may be important constrictor agonists, whereas nitric oxide is now considered to contribute to tonic reduction in vascular resistance. Little is known of the relative contributions of these vasoactive agents in the elevation of fetoplacental vascular resistance, but recent evidence points to an important role for altered vascular structure in growth-retarded pregnancies.

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Angiotensin-converting enzyme activity and contractile effects of angiotensin I and II in human uteroplacental arteries

Cited by 26 publications

References 30 publications

Captopril Reverses the Reduced Vasodilator Response to Bradykinin in Hypertensive Pregnant Rats

Captopril Reverses the Reduced Vasodilator Response to Bradykinin in Hypertensive Pregnant Rats

Autoradiographic Localization and Characterization of Angiotensin II Receptors in the Bovine Placenta and Fetal Membranes1

The control of blood flow to the placenta

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