Complete Contraction to Endothelin-1 in Endotoxin-Pretreated Rat Pulmonary Artery is Dependent on An Endothelium-Derived Cyclooxygenase Product

1995 ◽  
Vol 88 (s32) ◽  
pp. 27P-28P
Author(s):  
NP Curzen ◽  
MJ Griffiths ◽  
TW Evans ◽  
PA Kelly
Keyword(s):  
Pulmonary Artery ◽  
Endothelin 1 ◽  
Complete Contraction

Contraction to endothelin-1 in pulmonary arteries from endotoxin-treated rats is modulated by endothelium

1995 ◽  
Vol 268 (6) ◽  
pp. H2260-H2266
Author(s):  
N. P. Curzen ◽  
M. J. Griffiths ◽  
T. W. Evans
Keyword(s):  
Pulmonary Artery ◽  
Receptor Antagonist ◽  
Contractile Response ◽  
Pulmonary Arteries ◽  
The Novel ◽  
Receptor Stimulation ◽  
Thromboxane A2 Receptor ◽  
Endothelin 1 ◽  
Etb Receptor ◽  
Potent Vasoconstrictor

Sepsis is characterized by hyporesponsiveness of vascular smooth muscle to pressor agents. Levels of the potent vasoconstrictor, endothelin-1 (ET-1), are elevated in animal models of sepsis and in patients. This study assesses the contractile response of pulmonary artery from endotoxin-pretreated rats to ET-1 to determine whether this contraction is modified by the endothelium. Both intact and denuded rings from endotoxin-pretreated rats exhibited hyporesponsiveness to ET-1, but the endothelium was found to be essential for maximal ET-1-induced contraction. Upon pretreatment of vessels with the cyclooxygenase inhibitor, indomethacin (10(-5) M), the novel ETB-receptor antagonist, BQ-788 (10(-8) and 10(-6) M), and the thromboxane A2-receptor antagonist, ICI-192605 (10(-5) M), each of these agents caused a reduction in the ET-1-induced contraction of endotoxin-pretreated rat pulmonary artery only in the presence of the endothelium but had no effect in endothelium-denuded vessels or in sham-treated groups. These findings demonstrate that ET-1-induced contraction in pulmonary arteries from septic rats is partially dependent upon an endothelially derived cyclooxygenase product, the release of which appears to involve ETB-receptor stimulation.

Endothelin-1-induced potentiation of adrenergic responses in the rabbit pulmonary artery: role of thromboxane A2

2001 ◽  
Vol 413 (2-3) ◽  
pp. 247-254 ◽  
Author(s):  
José M. Vila ◽  
Pascual Medina ◽  
Gloria Segarra ◽  
Martı́n Aldasoro ◽  
Inmaculada Noguera ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Thromboxane A2 ◽  
Rabbit Pulmonary Artery ◽  
Endothelin 1

scholarly journals Profile of Endothelin-1, Nitric Oxide, and Prostacyclin Levels in Pulmonary Arterial Hypertension Related to Uncorrected Atrial Septal Defect: Results from a Single Center Study in Indonesia

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Lucia Kris Dinarti ◽  
Anggoro Budi Hartopo ◽  
Dyah Wulan Anggrahini ◽  
Ahmad Hamim Sadewa ◽  
Budi Yuli Setianto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arterial Hypertension ◽  
Plasma Level ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Atrial Septal Defect ◽  
Pulmonary Artery Pressure ◽  
Septal Defect ◽  
Endothelin 1 ◽  
Pulmonary Arterial

Background and Objectives. Pulmonary arterial hypertension (PAH) pathomechanism involves an increased plasma level of endothelin-1 and a reduced plasma level of prostacyclin and nitric oxide. Whether similar mechanisms prevail in PAH associated with atrial septal defect (ASD) is unclear. This study aimed to investigate the relationship of endothelin-1, prostacyclin, and nitric oxide with PAH in uncorrected ASD in Indonesian population. Methods. The study design was cross-sectional. The subjects were adult uncorrected secundum ASD with PAH. Pulmonary artery pressure was measured with right heart catheterization. Pulmonary venous blood was obtained during catheterization for measuring endothelin-1, prostacyclin, and nitric oxide. Correlation tests were performed to determine any association between biomarkers and mean pulmonary artery pressure (mPAP). The levels of biomarkers were compared based on the severity of PAH. Statistical significance was determined at p<0.05. Results. Forty-four subjects were enrolled in this study. Endothelin-1 level and mPAP had significant moderate positive correlation (r = 0.423 and p value = 0.004). However, no significant correlation was observed between prostacyclin, nitric oxide levels, and mPAP. The pattern of endothelin-1, prostacyclin, and nitric oxide was distinctive. Levels of endothelin-1 were incrementally increased from mild, moderate, to severe PAH. The levels of prostacyclin and nitric oxide had similar pattern in association with the severity of PAH, which was increased in mild-to-moderate PAH but decreased in severe PAH. Conclusions. There was a distinctive pattern of endothelin-1, prostacyclin, and nitric oxide based on severity of PAH in adult uncorrected ASD. Significant correlations existed between endothelin-1 and the severity of PAH and mPAP.

Resolvin D1 reverses reactivity and Ca2+ sensitivity induced by ET-1, TNF-α, and IL-6 in the human pulmonary artery

2014 ◽  
Vol 307 (11) ◽  
pp. H1547-H1558 ◽  
Author(s):  
Roddy Hiram ◽  
Edmond Rizcallah ◽  
Chantal Sirois ◽  
Marco Sirois ◽  
Caroline Morin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Contractile Activity ◽  
Transmembrane Protein ◽  
Pulmonary Arteries ◽  
Resolvin D1 ◽  
Endothelin 1 ◽  
Inflammatory Status ◽  
Tnf Α

Pulmonary hypertension (PH) is a rare and progressive disease characterized by an inflammatory status and vessel wall remodeling, resulting in increased pulmonary artery resistance. During the last decade, treatments have been proposed; most of them target the endothelial pathways that stimulate smooth muscle cell relaxation. However, PH remains associated with significant morbidity. We hypothesized that inflammation plays a crucial role in the severity of the abnormal vasoconstriction in PH. The goal of this study was to assess the effects of resolvin D1 (RvD1), a potent anti-inflammatory agent, on the pharmacological reactivity of human pulmonary arteries (HPAs) via an in vitro model of induced hyperreactivity. The effects of RvD1 and monoacylglyceride compounds were measured on contractile activity and Ca2+ sensitivity developed by HPAs that had been pretreated (or not) under proinflammatory conditions with either 10 ng/ml TNF-α or 10 ng/ml IL-6 or under hyperreactive conditions with 5 nM endothelin-1. The results demonstrated that, compared with controls, 24-h pretreatment with TNF-α, IL-6, or endothelin-1 increased reactivity and Ca2+ sensitivity of HPAs as revealed by agonist challenges with 80 mM KCl, 1 μM serotonin (5-hydroxytryptamine), 30 nM U-46619, and 1 μM phorbol 12,13-dibutyrate. However, 300 nM RvD1 as well as 1 μM monoacylglyceride-docosapentaenoic acid monoglyceride strongly reversed the overresponsiveness induced by both proinflammatory and hyperreactive treatments. In pretreated pulmonary artery smooth muscle cells, Western blot analyses revealed that RvD1 treatment decreased the phosphorylation level of CPI-17 and expression of transmembrane protein member 16A while increasing the detection of G protein-coupled receptor 32. The present data demonstrate that RvD1, a trihydroxylated docosahexaenoic acid derivative, decreases induced overreactivity in HPAs via a reduction in CPI-17 phosphorylation and transmembrane protein member 16A expression.

Contractile Actions of Endothelin-1 in Isolated Helical Strips from Rat Pulmonary Artery

1992 ◽  
Vol 20 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Hiroo Itoh ◽  
Naoto Hiraoka ◽  
Haruyuki Higuchi ◽  
Masaaki Ito ◽  
Tokuji Konishi ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Endothelin 1
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