Vasoactivity of the rat endovascular trophoblast

- EVasT react to ET1 like SM of non-modified arteries: contract via ETA and ETB and relax via ETB through NOS activation.
- Vascular rings of rat remodeled spiral artery contract ex vivo by blocking constitutive NOS in EVasT.
- ET1 induces earlier contraction of remodeled spiral artery in the presence of NOS inhibitor l-NAME.
- Precontracted vascular rings of rat remodeled spiral artery dilate ex vivo following exposure to NO donor SNAP.
- Potassium chloride (KCl) causes contraction of remodeled spiral artery ring ex vivo similar to non-remodeled arteries.

IntroductionRat endovascular trophoblasts (EVasT) express smooth muscle (SM) proteins and contract ex vivo upon exposure to endothelin-1 (ET1) via receptors A and B (ETA, ETB). Presently, we investigated the EVasT response to NOS inhibition (N-Nitro-l-arginine methyl ester hydrochloride, l-NAME), and potentiation by NO donor [S-Nitroso-N-Acetyl-D,l-Penicillamine (SNAP)] following KCl precontraction.M&MLuminal surface area (LSA) of remodeled spiral artery rings (SAR) devoid of SM was measured ex vivo upon exposure to l-NAME alone; l-NAME and ET1 representing the combined contractile effect of both ET1 receptors; l-NAME with ET1 and ETA antagonist, representing the isolated contractile effect via ETB. In another experiment we administered SNAP to KCl precontracted SAR. Statistical analysis was performed using 2-way mixed ANOVA and repeated measures.Resultsl-NAME reduced LSA by 2.22%, 95% CI [0.83%, 3.60%] compared with control. ET1 and l-NAME reduced LSA immediately, compared with a plateau at 60min by ET1 alone. The isolated ET1 constrictive effect via ETB, reduced LSA by 5.94%; 95% CI [3.47%, 8.41%], significantly more than that obtained via ETA following 36 min of the experiment by 0.88%; 95%CI [0.09%, 1.67%]. Addition of KCl reduced LSA by 11.9%, 95% CI [9.6%, 14.1%]. Addition of SNAP increased LSA by 3.0%, 95% CI [1.7%, 4.3%].ConclusionsEVasT of the rat remodeled spiral artery react to ET1 and KCl similar to vascular SM: contract via both ET1 receptors and KCl and relax by ET1 via ETB and by SNAP. This phenomenon may play a role in rat models of gestational vasoactive systems dysregulation.