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Urocortin-2 improves pulmonary endothelial function in experimental pulmonary arterial hypertension
Session:
Posters 1 - Écran 08 - HTA / Fármacos /Ciência Básica
Speaker:
Rui Miguel da Costa Adão
Congress:
CPC 2018
Topic:
O. Basic Science
Theme:
36. Basic Science
Subtheme:
36.4 Basic Science - Vascular Biology and Physiology
Session Type:
Posters
FP Number:
---
Authors:
Rui Adão; Luís Pimentel; Pedro Mendes-Ferreira; Carolina Maia-Rocha; Cláudia Pinto; Adelino Leite-Moreira; Carmen Brás-Silva
Abstract
<p>Pulmonary arterial hypertension (PAH) is a devastating disease and treatment options are limited. Urocortin-2 (Ucn-2) has shown promising therapeutic effects in experimental and clinical left ventricular heart failure (HF). Our aim was to investigate the effects of chronic and acute human Ucn-2 (hUcn-2) administration in the pulmonary endothelial function and vascular structure in experimental PAH.</p> <p>Wistar rats randomly received monocrotaline (MCT,60mg/Kg,sc) and, after 14 days, were treated with hUcn-2 (5ug/kg,bi-daily,i.p.,10 days) or vehicle. The study resulted in 4 groups: control (C,n=15); CTRL+hUcn-2 (CU,n=15); MCT (M,n=20); MCT+hUcn-2 (MU,n=20). Pulmonary arterial rings were isolated and mounted in a myograph system (720MO,DMT). For the acute vasodilatory tests, arterial rings were contracted with phenylephrine (phe,10<sup>-5</sup>M), and a dose-response to hUcn-2 (10<sup>-9</sup> to 5·10<sup>-7</sup> M) was performed. For the acute vasoconstriction-inhibiting effects, the arterial rings were firstly incubated with 50nM hUcn-2, and then contracted with phe. Endothelial function was assessed by attaining a dose–response curve to acetylcholine (10<sup>-9</sup> to 10<sup>-5</sup>M) after pre-contraction with phe. For histological analysis, samples were stored in buffered 10% formaldehyde. </p> <p>Pulmonary small artery remodeling was decreased in MU group compared to M, as measured by a decline in arteriole wall thickness. Isolated pulmonary arterial rings from control and MCT rats pre-contracted with phe, exhibited a vasodilation response when incubated with hUcn-2. The vasodilation response to hUcn-2 was independent of the endothelium. Furthermore, pre-treatment with hUcn-2 attenuated phenylephrine-induced vasoconstriction in arterial rings isolated from control animals, while there was no inhibitory effect in the MCT group. We found a lack of relaxation in a dose–response test to acetylcholine in pulmonary arteries isolated from MCT animals and treating chronically animals with hUcn-2 significantly increased the maximal response to acetylcholine. Furthermore, hUcn-2 decreased the EC50 showing increased receptor sensitivity to acetylcholine.</p> <p>hUcn-2 treatment attenuates vascular remodeling in MCT-induced PAH and improves pulmonary vascular function. Acute hUcn-2 effects in pulmonary arterial rings demonstrated a significant endothelium-independent vasodilatory effect. This can be an advantage in PAH which is associated with impaired endothelial homeostatic mechanisms.</p>
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