-adrenergic relaxation in pulmonary arteries: preservation of the endothelial nitric oxide-dependent  2 component in pulmonary hypertension

Leblais, Véronique; Delannoy, E; Fresquet, Fleur; Bégueret, Hugues; Bellancé, Nadège; Banquet, Sébastien; Allières, Cécile; Leroux, Lionel; Des̀granges, Claude; Gadeau, Alain Pierre; Müller, Bernard

doi:10.1093/cvr/cvm008

Cited by 48 publications

(53 citation statements)

References 37 publications

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“…Endothelial β 2 -AR stimulation elicits a NO-dependent relaxant response in both systemic [7][8][9] and pulmonary [6] vasculature. However, the molecular mechanisms involved in the coupling of β 2 -ARs to eNOS activation remained poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…In a previous study, we have shown that in mouse pulmonary artery precontracted by PGF 2α , 0.1 µM procaterol (in the presence of phentolamine) induces a relaxation which is exclusively due to the endothelial β 2 -AR, eNOS and soluble guanylyl-cyclase stimulation [6].…”

Section: Role Of G I/o Proteins In the β 2 -Ar-mediated Relaxant Respmentioning

confidence: 93%

“…In a mouse model of chronic hypoxia-induced pulmonary arterial hypertension, we have shown that the relaxant response induced by the β 2 -AR stimulation, which is also endothelium-and eNOSdependent, is preserved, whereas the relaxant response to acetylcholine is decreased [5,6].…”

Section: Introductionmentioning

confidence: 94%

“…Segments of pulmonary arteries were mounted in a wire myograph (Multi Myograph System, model 610M, J.P. Trading, Aarhus, Denmark) to measure isometric tension, as previously described [5,6]. Relaxant effects of 10 µM acetylcholine and 0.1 µM procaterol (in the presence of the α-adrenoceptor antagonist phentolamine, 10 µM) were studied in the same artery, after submaximal pre-contraction with PGF 2α .…”

Section: Vascular Reactivity Studiesmentioning

confidence: 99%

“…Whereas in mouse pulmonary arteries muscarinic-dependent activation of eNOS involves the M 3 subtype [14], which is coupled to a G q /phospholipase C pathway and subsequent increase in cytosolic calcium concentration in endothelial cells, it is worth noting that the coupling mechanism between β 2 -AR and eNOS remains unknown in these arteries, except that it is independent of a cAMP/cAMP-dependent protein kinase (PKA) pathway [6], suggesting that G s proteins are not recruited.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery

Banquet

Delannoy

Agouni

et al. 2011

Cellular Signalling

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Section: Discussionmentioning

confidence: 99%

Section: Role Of G I/o Proteins In the β 2 -Ar-mediated Relaxant Respmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 94%

Section: Vascular Reactivity Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery

Banquet

Delannoy

Agouni

et al. 2011

Cellular Signalling

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Role of PKCζ‐NADPH oxidase signaling axis in PKCα‐mediated Giα2 phosphorylation for inhibition of adenylate cyclase activity by angiotensin II in pulmonary artery smooth muscle cells

Chowdhury

Sarkar

Pramanik

et al. 2020

Cell Biology International

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We sought to determine the mechanism by which angiotensin II (AngII) inhibits isoproterenol induced increase in adenylate cyclase (AC) activity and cyclic adenosine monophosphate (cAMP) production in bovine pulmonary artery smooth muscle cells (BPASMCs). Treatment with AngII stimulates protein kinase C-ζ (PKC-ζ), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and PKC-α activities, and also inhibits isoproterenol induced increase in AC activity and cAMP production in the cells. Pertussis toxin pretreatment eliminates AngII caused inhibition of isoproterenol induced increase in AC activity without a discernible change in PKC-ζ, NADPH oxidase, and PKC-α activities. Treatment of the cells with AngII increases α2 isoform of Gi (Giα2) phosphorylation; while pretreatment with chemical and genetic inhibitors of PKC-ζ and NADPH oxidase attenuate AngII induced increase in PKC-α activity and Giα2 phosphorylation, and also reverse AngII caused inhibition of isoproterenol induced increase in AC activity. Pretreatment of the cells with chemical and genetic inhibitors of PKC-α attenuate AngII induced increase in Giα2 phosphorylation and inhibits isoproterenol induced increase in AC activity without a discernible change in PKC-ζ and NADPH oxidase activities. Overall, PKCζ-NADPH oxidase-PKCα signaling axis plays a crucial role in Giα2 phosphorylation resulting in AngII-mediated inhibition of isoproterenol induced increase in AC activity in BPASMCs.

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Nonpulmonary Influences on Gas Exchange

Rodríguez-Roisin

2014

Comprehensive Physiology

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There are several determinants governing arterial and mixed venous blood PO2 and PCO2. Ventilation-perfusion imbalance, increased intrapulmonary shunt, and diffusion limitation to oxygen encompass the pulmonary factors. Alternatively, inspired oxygen concentration, overall ventilation, cardiac output, and oxygen consumption (uptake) are contemplated as the four most influential nonpulmonary determinants. All three pulmonary factors plus oxygen uptake cannot be directly modulated, but all the other remaining nonpulmonary determinants are. Inspired oxygen concentration, the amount and pattern of total ventilation, and cardiac output may be, at least in part, relatively well clinically controlled. Arterial PO2 (PaO2) may fall if inspired PO2, overall ventilation, and/or cardiac output decrease, and/or oxygen consumption increases, even though the pulmonary factors remain unchanged. Conversely, if inspired oxygen fraction, ventilation, and/or cardiac output increase, and/or oxygen consumption decreases, PaO2 may improve regardless of the changes operated at the level of the pulmonary determinants. Several pathophysiologic features deserve to be underlined. First, the importance of understanding the role played by mixed venous PO2 as a vital nonpulmonary determinant governing PaO2. Second, the response to 100% oxygen breathing repeatedly exhibits a consistent amount of agreement in the main findings. Third, there is always an interactive interplay between pulmonary and nonpulmonary determinants of PaO2 and arterial PCO2 (PaCO2) in any respiratory disease state following the use of pharmacologic or nonpharmacologic approaches. All in all both PaO2 and PaCO2 become the end-point outcomes of the complex interaction of pulmonary and nonpulmonary factors modulating pulmonary gas exchange. This needs to be unraveled to improve the understanding and management of most acute and chronic respiratory disease states.

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-adrenergic relaxation in pulmonary arteries: preservation of the endothelial nitric oxide-dependent 2 component in pulmonary hypertension

Cited by 48 publications

References 37 publications

Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery

Role of Gi/o-Src kinase-PI3K/Akt pathway and caveolin-1 in β2-adrenoceptor coupling to endothelial NO synthase in mouse pulmonary artery

Role of PKCζ‐NADPH oxidase signaling axis in PKCα‐mediated Giα2 phosphorylation for inhibition of adenylate cyclase activity by angiotensin II in pulmonary artery smooth muscle cells

Nonpulmonary Influences on Gas Exchange

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