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Investigating the role of the two pore domain potassium channel TWIK related K2P in placental vessels
  1. TY Ali1,
  2. F Broughton Pipkin1,2,
  3. RN Khan1
  1. 1Derby Medical School, University of Nottingham, Derby, UK
  2. 2Department of Obstetrics and Gynaecology, University of Nottingham, Nottingham, UK

Abstract

The placenta needs to maintain a low resistance system to deliver sufficient oxygen and nutrients to the fetus. Blood vessels within the placenta respond to challenges in maternal blood supply by altering the vessel diameter but the exact nature of the ion channels involved in this response are not known. The two pore domain potassium (K2P) channel TWIK related K2P (TREK-1) has shown to be important in controlling vessel tone and the authors aim to study the function of TREK-1 in placental vessels. Placentae were collected with written consent from patients undergoing elective Caesarean section at term (≥37 weeks). Smooth muscle cells (SMC) were cultured from the chorionic plate (CPA) and stem villous (SVA) arteries in order to compare vessels found across the placenta. Cells were immunostained for TREK-1 and images were captured with a Leica confocal microscope. Arteries (200–500 μm) taken from the CPA and SVA were studied using wire myography. Vessels were first contracted with U46619 (10−12 to 10−6 M) before the TREK-1 opener riluzole (10−10 to 10−6 M) was added. SMC from CPA and SVA were positive for the expression of TREK-1 and showed co-localisation with α actin (Pearson co efficient 0.86±0.48). Stimulation of isolated vessels with riluzole produced a potent vasodilatation. A maximum relaxation of 52.45%±7.19% and 48.9%±11.05% at 10−6 M was achieved in the CPA (n=10) and SVA (n=6) vessels. These findings implicate TREK-1 in controlling the vasodilatation of placental arteries. The authors suggest that K2P channels are a potential target for treating disorders that result in placental tissue to become poorly perfused.

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