Effects of Some Autacoids and Humoral Agents on Human Fetoplacental Vascular Resistance: Candidates for Local Regulation of Fetoplacental Blood Flow (original) (raw)

Springer eBooks, 1988

Abstract

Mechanisms of local regulation of blood flow through the extensive fetoplacental vascular bed of the mature human placenta are not understood. As the placenta is not innervated, there is no nervous control of vascular resistance. Locally-produced vasoactive autacoids such as prostaglandins and thromboxane could play a role in modulating fetoplacental blood flow, or humoral agents could be involved. Human placenta in the form of in vitro slice preparations has been shown to produce thromboxane B2, the stable metabolite of thromboxane A2, and to convert exogenous arachidonic acid to several prostanoids, including PGE2, PGD2, PGF2α and 6-keto-PGF1α a biologically inactive metabolite of prostacyclin, PGI2 (Mitchell et al., 1982; Makila et al., 1984; Harper et al., 1983). Also, higher levels of iPGE were found in umbilical venous plasma than in plasma from umbilical arteries (Bibby et al., 1979), suggesting that production of PGE by the placenta occurs in vivo. Thromboxane A2, PGE2, and PGI2 are known to have pressor or depressor actions in many vascular beds (Whittle and Moncada, 1984; Kadowitz et al., 1984). We therefore evaluated the effects of PGE2, PGF2α, PGI2, PGE1 and the endoperoxide analogue U46619, a thromboxane mimetic (Granstrom et al., 1983), on the resistance of human fetoplacental vasculature in isolated dual-perfused cotyledons from human term placenta. Furthermore, the formation of a potentially important humoral agent, angiotensin II (AII), within the fetoplacental vascular bed was studied.

Alan Poisner hasn't uploaded this paper.

Let Alan know you want this paper to be uploaded.

Ask for this paper to be uploaded.