Evidence for a functional renin-angiotensin system in full-term fetoplacental unit

Abstract

This investigation was performed to study the renin-angiotensin system in the human fetoplacental circulation. Full-term placentas from uncomplicated pregnancies were studied within 30 min of delivery. The umbilical artery and vein to a single placental cotyledon were cannulated and the artery perfused with RPMI media (0.764 ml/min). Angiotensin II caused a dose-dependent increase in perfusion pressure that was blunted by the administration of the competitive angiotensin II receptor antagonist saralasin. The properties of human placental angiotensin II receptors were further defined in binding studies performed on a crude membrane fraction of placental cotyledons. In experiments performed at 22 degrees C, saturable binding reached steady state at 30 min and was linear with protein concentration. Scatchard analysis of binding data indicated a single class of high-affinity binding sites. The potency order to competitive binding of analogues and antagonists of angiotensin II was [Ile5]angiotensin II = [Sar1, Ala8]-angiotensin II greater than [Val5]angiotensin II greater than angiotensin III greater than angiotensin II-(3-8) hexapeptide. Further evidence for the physiological significance of angiotensin II binding sites was provided by measurements of the circulating components of the renin-angiotensin system in umbilical venous blood (n = 7). Plasma renin activity, angiotensin I, angiotensin-converting enzyme activity, angiotensin II, and aldosterone were each present in elevated amounts. These experiments provide evidence for an active renin-angiotensin system in the human fetal circulation that may modulate placental perfusion and function under physiological conditions.

Salt intake and reproductive function in sheep

“…For example, Digby, Chadwick and Blache angiotensin II partly regulates the blood flow in the uteroplacental unit, and thereby indirectly influences the fetal volume homeostasis and oxygenation (Wilkes et al, 1985). The RAS of the mother is essential to the maintenance of the fetal glomerular filtration rate (Lumbers et al, 1996).…”

Altered release of endothelin‐1,2 and thromboxane B2 from trophoblastic cells in pre‐eclampsia

“…The human placenta contains a complete reninangiotensin system [8,9], receptors for angiotensin II [10,11] and four times more angiotensin II than umbilical and maternal blood at term [11]. Contradictory reports exist about changes in plasma levels of endothelin-1 in pregnancies complicated by preeclampsia; both an increase [12] and no change [13] in ET-1 plasma concentrations have been found.…”

Les récepteurs de l'angiotensine II dans le placenta humain sont de type AT1

“…En outre, il a été démontré que l'angiotensine Il stimule la sécrétion de l'hormone placentaire lactogène (hPL) par des cellules trophoblastiques , la sécrétion de la prolactine par des cellules adénohypophysaires (Platia et al, 1986;Myers et Steele, 1989) et la biosynthèse des hormones stéroïdes par les cellules de la granulosa (Pucell et al, 1987;Guichard et al, 1988;Palumbo et al, 1989 (Cooke et al, 1981;Wilkes et al, 1985;Kurauchi et al, 1990 (Munson et Rodbard, 1980;Whitebread et al, 1989) (Whitebread et al, 1989).…”

“…Une certaine confusion existe dans la littérature (Chiu et al, 1989;Chang et (Criscione et al, 1990;de Gasparo et al, 1990 (Cooke et al, 1981;Wilkes et al, 1985; Kurauchi et al, 1990) …”