Renin, Angiotensin II, Aldosterone, Catecholamines, Prostaglandins and Vasopressin. The Importance of Pressor and Depressor Factors for Hypertension in Pregnancy

Eb, Pedersen; Aalkjær, Christian; Nj, Christensen; Christensen, Poul; Danielsen, H.; Johannesen, P.; Hj, Kornerup; Pp, Leyssac; Mulvany, Michael J.; Ab, Rasmussen

doi:10.3109/00365518409085377

Cited by 13 publications

(7 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a previous study [8] we found the same AVP level during normal pregnancy and in nonpregnant control subjects as in the present study. As in the present study, how ever, others have found high concentrations of AVP in umbilical arterial cord blood at the time of birth [3,5,9] and animal experiments have shown that the fetus is autonomic with respect to AVP secretion and the placenta impermeable to AVP [1,10,11], Hadeed et al [12] have suggested that intracranial pres sure elevation resulting from labor and birth stimulates AVP secretion in the fetus.…”

Section: Discussionsupporting

confidence: 58%

Arginine Vasopressin in Amniotic Fluid, Arterial and Venous Cord Plasma and Maternal Venous Plasma

Johannesen¹,

Pedersen²,

Rasmussen³

1985

Gynecol Obstet Invest

View full text Add to dashboard Cite

High concentrations of arginine vasopressin (AVP) in arterial umbilical cord blood at the time of delivery have been attributed to either a generalized increase in the activity of the fetal endocrine system at the onset of labor or to fetal asphyxia. We measured AVP in amniotic fluid, arterial and venous cord blood and in maternal venous blood from 13 patients at 38–40 weeks of gestation at the time of elective cesarean section with a nonasphyxic fetus (group I), in amniotic fluid from 19 patients at 15–17 weeks of gestation (group II) and in venous blood from 13 nonpregnant control subjects (group III). Our results showed a high concentration of AVP in the amniotic fluid both in the middle and at the end of normal pregnancy and at the same level as in arterial cord blood, whereas AVP in the venous cord blood was significantly lower and at the same level as in the maternal venous blood and in the control group. It is concluded that the fetus produces AVP and this is at least not solely caused by fetal asphyxia or related to parturition.

show abstract

Section: Discussionsupporting

confidence: 58%

Arginine Vasopressin in Amniotic Fluid, Arterial and Venous Cord Plasma and Maternal Venous Plasma

Johannesen¹,

Pedersen²,

Rasmussen³

1985

Gynecol Obstet Invest

View full text Add to dashboard Cite

show abstract

“…this biological effect in the maternal circulation, and the focus over the years has encompassed the reninangiotensin system [57][58][59][60][61], norepinephrine [62,63], vasopressin [64], prostaglandins [65], endothelin [20], cytokines [7], and others [66]. Since many investigators believed that the placenta is the source of the pressor agents, some studies also explored the concentration of numerous candidate mediators for 'toxic factors' of preeclampsia in the uterine vein, which represents blood exiting the uterus before gaining access to the peripheral circulation.…”

Section: Discussionmentioning

confidence: 99%

Evidence supporting that the excess of the sVEGFR-1 concentration in maternal plasma in preeclampsia has a uterine origin

Bujold

Romero

Chaiworapongsa

et al. 2005

The Journal of Maternal-Fetal & Neonatal Medicine

105

View full text Add to dashboard Cite

(2005) Evidence supporting that the excess of the sVEGFR-1 concentration in maternal plasma in preeclampsia has a uterine origin, The Journal of 18:1,[9][10][11][12][13][14][15][16] Abstract Background. Preeclampsia has been considered an anti-angiogenic state. Two factors have been implicated in the genesis of this state: soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) and placental growth factor (PlGF). Indeed, the concentrations of PlGF, an angiogenic factor, are lower in preeclampsia than in normal pregnancy, while the opposite is the case for the anti-angiogenic factor, sVEGFR-1. The source of the excess sVEGFR-1 has not yet been determined. Since the placenta could be a source of sVEGFR-1, we conducted a study to determine whether there is a gradient in the plasma concentration of sVEGFR-1 and PlGF between the uterine vein and the antecubital vein in both patients with preeclampsia and normal pregnant women. Methods. A cross-sectional study was performed to determine the plasma concentrations of sVEGFR-1 and PlGF in the uterine and antecubital vein of patients with preeclampsia (n = 9) and normal pregnant women at term (n = 9). Plasma samples were collected from antecubital and uterine veins at the time of cesarean section. The concentrations of sVEGFR-1 and PlGF were determined using specific enzyme-linked immunoassays. The differences of plasma concentrations of sVEGFR-1 and PlGF between uterine and antecubital veins in both groups were compared by paired t-tests. Results. Patients with preeclampsia had a significantly higher mean plasma concentration of sVEGFR-1 in the uterine vein than in the antecubital vein (uterine vein: mean 13,675 + 5,684 pg/ml vs. antecubital vein: mean 10,234 + 4,700 pg/ml; paired t-tests, p = 0.04). In contrast, among normal pregnant women at term, there was no significant difference in plasma concentrations of sVEGFR-1 between the uterine and antecubital veins (uterine vein: mean 1,918 + 665 pg/ml vs. antecubital vein: mean 1,750 + 475 pg/ml; paired t-tests, p = 0.1). The mean plasma concentration of sVEGFR-1, either in the antecubital or uterine vein, was significantly higher in preeclampsia than in normal pregnancy (unpaired t-tests; both p 5 0.001). There was no significant difference in the mean plasma concentration of PlGF between the uterine and the antecubital veins in both the preeclamptic (uterine vein, mean + SD: 129 + 106 pg/ml vs. antecubital vein, mean + SD: 82 + 43 pg/ml; paired t-tests, p = 0.2) and normal pregnancy groups (uterine vein, mean + SD: 331 + 254 pg/ml vs. antecubital vein, mean + SD: 319 + 259 pg/ml; paired t-tests, p = 0.4). The mean plasma concentration of PlGF, either in the uterine or antecubital vein, was lower in preeclampsia than in normal pregnancy (unpaired t-tests; p = 0.008 and 0.02 respectively). Conclusions. Plasma concentration of sVEGFR-1 was higher in the uterine vein than in the antecubital vein in women with preeclampsia. This provides evidence supporting the concept that the uterus is a potential source of the ...

show abstract

“…Since the increase in blood pressure could not be elicited by re-transfusion 6 weeks postpartum, the authors concluded that patients with pre-eclampsia had increased sensitivity to pressor agent(s) which lasted about 1 week after delivery, but not as long as 6 weeks. Thereafter, considerable effort was devoted to the identification of the pressor agent responsible for this biological effect in the maternal circulation, and the focus over the years has encompassed the renin-angiotensin system [47][48][49][50] , noradrenaline (norepinephrine) 51,52 , vasopressin 53 , prostaglandins 54 , endothelin 55 and others 56 .…”

Section: Discussionmentioning

confidence: 99%

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Neale

Demasio

Illuzi

et al. 2003

The Journal of Maternal-Fetal & Neonatal Medicine

View full text Add to dashboard Cite

Renin, Angiotensin II, Aldosterone, Catecholamines, Prostaglandins and Vasopressin. The Importance of Pressor and Depressor Factors for Hypertension in Pregnancy

Cited by 13 publications

References 19 publications

Arginine Vasopressin in Amniotic Fluid, Arterial and Venous Cord Plasma and Maternal Venous Plasma

Arginine Vasopressin in Amniotic Fluid, Arterial and Venous Cord Plasma and Maternal Venous Plasma

Evidence supporting that the excess of the sVEGFR-1 concentration in maternal plasma in preeclampsia has a uterine origin

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Contact Info

Product

Resources

About