Endothelial hyperpolarizing factor increases acetylcholine-induced vasodilatation in pulmonary hypertensive broilers arterial rings

Alvarez-Medina, Diana I.; Hernández, Aureliano; Orozco, Camilo

doi:10.1016/j.rvsc.2011.02.004

Cited by 7 publications

(2 citation statements)

References 37 publications

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“…A considerable body of evidence suggests that the development of PAH results from increased pulmonary vascular resistance. − Cumulative evidence attributes the increased pulmonary vascular resistance to inadequacy of pulmonary vascular capacity to accommodate ever-increasing cardiac output required to meet oxygen demands for rapid growth, , and to imbalance between vasoconstrictors and vasodilators. − Structural remodeling of small pulmonary arteries characterized by medial hypertrophy and intimal hyperplasia also leads to increased vascular resistance. − Plexogenic arteriopathy, which might result from dysfunction of endothelial progenitor cells (EPCs), has been recently implicated in the pathogenesis of PAH. , In addition, several lines of evidence suggest that the onset of PAH is associated with oxidative stress − and environmental and genetic factors . In general, these studies have provided rich data sets on PAH.…”

Section: Introductionmentioning

confidence: 99%

Metabonomics Profiling Reveals Biochemical Pathways Associated with Pulmonary Arterial Hypertension in Broiler Chickens

et al. 2018

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Pulmonary arterial hypertension (PAH) is the major cause of death in fast growing meat-type chickens (broiler chickens). At present, the underlying mechanisms that give rise to PAH are not fully understood. To identify the metabonomics profiles characterizing the process, we conducted a comprehensive gas chromatography-mass spectrometry (GC-MS)-based metabolic profiling of lung tissues from PAH broilers and age-matched controls. PAH was induced by excess salt in drinking water. Medial hypertrophy of pulmonary arteries was present in PAH birds as compared with controls. The metabonomics profiles of lung tissues well distinguished PAH broilers from control subjects. Significant changes in the levels of 41 metabolites were detected in PAH vs normal birds. Aside from the metabolic alterations indicating a status of oxidative stress and inflammation, evidence of reduced cellular uptake of arginine due to increased lysine biosynthesis and of a shift of arginine metabolism to arginase pathway were observed. In addition, PAH birds showed increased biosynthesis of fatty acids, which may be associated with excessive proliferation of vascular cells during pulmonary vascular remodeling. Furthermore, we observed significant changes in pentose phosphate pathway and increased aminomalonic acid in PAH broilers. These results provide additional biochemical insights into the pathogenesis of the PAH. Our data may lead to the development of new strategies to control PAH in broilers.

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Section: Introductionmentioning

confidence: 99%

Metabonomics Profiling Reveals Biochemical Pathways Associated with Pulmonary Arterial Hypertension in Broiler Chickens

et al. 2018

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“…This may be simply due to species and tissue difference. For example, AA causes significant vessel contraction in human pulmonary vein and AA infusion triggers marked, sustained pulmonary vasoconstriction and pulmonary hypertension in broilers (19). The vasoconstriction effect of AA is endothelium dependent, since AA exerts no effect on denuded vessel rings.…”

Section: A B Cmentioning

confidence: 99%

Predominant role of vasoconstrictors over dilatators derived from arachidonic acid in hypoxic pulmonary vasoconstriction

Han

Yan

Wang

et al. 2013

Molecular Medicine Reports

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Prostanoids derived from arachidonic acid (AA) have been shown to play a permissive role in the regulation of vascular tone and wall tension. Conventionally, epoxyeicosatrienoic acids (EETs) and prostacyclin have been considered as dilatators, whereas thromboxane (TX) and hydroxyeicosatetraenoic acid (HETE) were considered as vasoconstrictors. However, the role of these prostanoids in the mediation of acute hypoxic pulmonary vasoconstriction is not yet clearly understood. In the present study, the role of prostanoids in the acute hypoxic response in rat isolated intrapulmonary arteries (IPAs) was investigated. Exogenous AA directly caused vasoconstriction, but exerted a significant inhibition on hypoxic vasoconstriction. The vasoconstriction by AA was mediated by the endothelium. AA metabolites from lipoxygenase (LOX) had no effect on vascular tone or hypoxic vasoconstriction. Consistent results from the blockage of cytochrome P450 (CYP) or CYP epoxide hydrolase showed that HETE contributed to endothelium‑independent hypoxic vasoconstriction. EET via epoxygenase exerted no effect on 80 mM KPSS‑induced vessel contraction or hypoxic vasoconstriction. In addition, prostacyclin also failed to inhibit hypoxic pulmonary vasoconstriction (HPV). However, blockage of thromboxane A2/prostanoid (TP) receptors almost eliminated hypoxic vasoconstriction, suggesting the primary role of TP receptors in the regulation of the hypoxic response in rat IPAs. In conclusion, the current data indicate the predominant role of vasoconstrictors instead of dilatators in mediating HPV. These data also highlight a pivotal role for voltage‑independent Ca2+ entry in pulmonary hypoxic response and suggest that modulation of these channels by prostanoids underlies their regulatory mechanisms.

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The evolution of nitric oxide signalling in vertebrate blood vessels

2014

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Nitric oxide is one of the most important signalling molecules involved in the regulation of physiological function. It first came to prominence when it was discovered that the vascular endothelium of mammals synthesises and releases nitric oxide (NO) to mediate a potent vasodilation. Subsequently, it was shown that NO is synthesised in the endothelium by a specific isoform of nitric oxide synthase (NOS) called NOS3. Following this discovery, it was assumed that an endothelial NO/NOS3 system would be present in all vertebrate blood vessels. This review will discuss the latest genomic, anatomical and physiological evidence which demonstrates that an endothelial NO/NOS3 signalling is not ubiquitous in non-mammalian vertebrates, and that there have been key evolutionary steps that have led to the endothelial NO signalling system being a regulatory system found only in reptiles, birds and mammals. Furthermore, the emerging role of nitrite as an endocrine source of NO for vascular regulation is discussed.

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Endothelial hyperpolarizing factor increases acetylcholine-induced vasodilatation in pulmonary hypertensive broilers arterial rings

Cited by 7 publications

References 37 publications

Metabonomics Profiling Reveals Biochemical Pathways Associated with Pulmonary Arterial Hypertension in Broiler Chickens

Metabonomics Profiling Reveals Biochemical Pathways Associated with Pulmonary Arterial Hypertension in Broiler Chickens

Predominant role of vasoconstrictors over dilatators derived from arachidonic acid in hypoxic pulmonary vasoconstriction

The evolution of nitric oxide signalling in vertebrate blood vessels

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