Abstract P177: The Myotrophoblast of the Rat Placenta Ex Vivo Study of Nitric Oxide Synthase Inhibition

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Ilana Ariel ◽  
Galina Skarzinski ◽  
Vitali Belzer ◽  
Wiessam Abu Ahmad ◽  
Zaid Abassi ◽  
...  

In pregnancy spiral arteries, are invaded by endovascular trophoblasts (EVT) and remodeled. Previously, NOS, and of smooth muscle proteins expression in EVT, and endothelin-1 (ET1) ex-vivo contraction of the remodeled artery were demonstrated, mediated by ET1 receptors A and B (ETA, ETB) Placentas on gestational day 21, were dissected, spiral artery rings devoid of smooth muscle were fixed to a silicon-coated 8-well chamber slide in oxygenated solution. Rings cut surface area (CSA) was observed under laser scanning confocal microscope. Following baseline, L-NAME and 10- 5 M, ET-1 10-7 M were added to some chambers. In other wells, also with ETA antagonist at 10-6 M (BQ-123). CSA was measured using ImageJ software. L-NAME alone, reduced CSA by 2.5% p=0.002. Addition of ET-1 to L-NAME, reduced CSA area immediately, compared with a plateau at 60min by ET1 p=0.001 .L-NAME, followed by ET-1 and ETA antagonist, the isolated constrictive effect of ET-1 via ETB, 7.2%, was earlier and stronger n than via ETA, 6.1% p< 0.001 (figure). L-NAME + ET-1 causes contraction of the arterial ring via ETA and ETB, without the dilatory effect of NO. ET-1 alone shows an earlier, immediate CSA reduction, compared to that of ET-1 without L-NAME, achieved at 40-60 minutes. This is in accordance with the instantaneous NO effect through ETB, compared with the gradual ET-1 induced CSA reduction .To isolate the contracting effect via ETB, we added L-NAME + ETA+ ET-1. The ETB contraction is earlier and stronger than that via ETA. Thus, EVT of the rat remodeled spiral artery react to ET-1 like vascular smooth muscle of non-modified arteries: contraction via receptors A and B and relaxation via receptor B through NOS.

2006 ◽  
Vol 116 (7) ◽  
pp. 1136-1141 ◽  
Author(s):  
Tino Just ◽  
Joachim Stave ◽  
Carsten Boltze ◽  
Andreas Wree ◽  
Burkhard Kramp ◽  
...  

2015 ◽  
Vol 12 (C) ◽  
pp. 19
Author(s):  
Ilana Ariel ◽  
Galina Skarzinski ◽  
Vitali Belzer ◽  
Wiessam Abu-Ahmad ◽  
Zaid Abassi ◽  
...  

1995 ◽  
Vol 74 (03) ◽  
pp. 980-986 ◽  
Author(s):  
Valérie B Schini-Kerth ◽  
Beate Fißithaler ◽  
Thomas T Andersen ◽  
John W Fenton ◽  
Paul M Vanhoutte ◽  
...  

SummaryProteolytically active forms of thrombin (α- and γ-thrombin) and thrombin receptor peptides inhibited the release of nitrite, a stable endproduct of nitric oxide, evoked by interleukin-1 β(IL-1 β) in cultured vascular smooth muscle cells while proteolytically inactive forms [D-Phe-Pro-Arg chloromethyl ketone-α-thrombin (PPACK-α- thrombin) and diisopropylphosphoryl-α-thrombin (DIP-α-thrombin)] had either no or only minimal inhibitory effects. Under bioassay conditions, perfusates from columns containing IL-1 β-activated vascular smooth muscle cells or cells treated with IL-1βplus PPACK-α-thrombin relaxed detector blood vessels. These relaxations were abolished by the inhibitor of nitric oxide synthesis, NG-nitro-L arginine. No relaxations were obtained with untreated cells or IL-1 β-treated cells in the presence of α-thrombin. The expression of inducible nitric oxide synthase mRNA and protein in vascular smooth muscle cells by IL-1 β was impaired by α-thrombin. These results demonstrate that thrombin regulates the expression of the inducible nitric oxide synthase at a transcriptional level via the proteolytic activation of the thrombin receptor in vascular smooth muscle cells


2020 ◽  
Author(s):  
Rafael Heiss ◽  
Frank W. Roemer ◽  
Christoph Lutter ◽  
Rolf Janka ◽  
Volker Schöffl ◽  
...  

2014 ◽  
Author(s):  
Klaus Engelke ◽  
Nicolas Bouler ◽  
Oleg Museyko Fuerst ◽  
Sebastien Parratte ◽  
Thomas Fuerst ◽  
...  

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