Regulation of endothelial permeability by β-adrenoceptor agonists: Contribution of β1- and β2-adrenoceptors

Zink, Sigrid; Rösen, P.; Sackmann, Beate; Lemoine, Horst

doi:10.1016/0167-4889(93)90206-5

Cited by 39 publications

(28 citation statements)

References 41 publications

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“…The existence of ␤ 2 -adrenoceptors on endothelial cells is in accordance with other studies (Zink et al, 1993). We show here, to our best knowledge for the first time, that hyperglycemia does not alter the density of ␤-adrenoceptors and does not change the ␤ 1 :␤ 2 ratio.…”

Section: Discussionsupporting

confidence: 78%

Effect of a β₂-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Kabat

Pönicke²,

Salameh³

et al. 2003

J Pharmacol Exp Ther

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To investigate whether ␤ 2 -adrenoceptors exist on endothelial cells and whether a ␤ 2 -adrenoceptor stimulation might prevent the development of hyperglycemia-induced endothelial dysfunction, porcine aortic endothelial cells (PAECs) were cultured and chronically exposed to either 5 mM D-glucose ("normoglycemia") or 20 mM D-glucose ("hyperglycemia"), with or without 100 nM salbutamol in absence or presence ofFor osmotic control, PAECs were exposed to 15 mM L-glucose. We measured nitric oxide release using the met-hemoglobin assay and assessed ␤-adrenoceptor density and subtypes by radioligand binding. Furthermore, we determined intracellular NADH and NADPH using high-performance liquid chromatography. High Dglucose concentrations but not L-glucose led to significantly reduced basal and stimulated nitric oxide release. Chronic salbutamol treatment significantly antagonized the impairment of the nitric oxide response, which was inhibited by ICI 118,551 but not by metoprolol. The number of giant cells was significantly increased in hyperglycemia, which could be prevented by salbutamol. Binding of the radioligand (Ϫ)-[ 125 I]iodocyanopindolol revealed a total ␤-adrenoceptor density of 29.8 Ϯ 3.7 (normoglycemic) and 30.3 Ϯ 3.6 (hyperglycemic) fmol/mg protein. Displacement by ICI 118,551 revealed ␤-adrenoceptor subtype distribution with 30.3 Ϯ 4.4 (normoglycemic) and 29.1 Ϯ 3.8% ␤ 2 -adrenoceptors. NADH production increased in hyperglycemia, which was completely prevented by salbutamol. We conclude that hyperglycemia in PAEC induces endothelial dysfunction with impaired nitric oxide release and that this can be prevented by ␤ 2 -adrenoceptor stimulation.An intriguing problem in antidiabetic therapy is the development of generalized angiopathy and concomitant hypertension in diabetes mellitus. The nature of the underlying processes is complex and not yet fully understood. Several lines of evidence suggest that vascular endothelial function is disturbed in diabetes (Fortes et al., 1983;Cagliero et al., 1991;Sank et al

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Section: Discussionsupporting

confidence: 78%

Effect of a β₂-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Kabat

Pönicke²,

Salameh³

et al. 2003

J Pharmacol Exp Ther

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“…many pro-inflammatory and immune cells, including mast cells [35], macrophages [36], neutrophils [37], lymphocytes [38], eosinophils [39], epithelial and endothelial cells [40,41], and both type I and type II alveolar cells [10,42,43]. Thus, many cell types within the lung that are implicated in the pathogenesis of asthma are potential targets of inhaled b 2 -adrenoceptor agonists.…”

Section: Adrenoceptors In the Lungmentioning

confidence: 99%

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Giembycz

Newton²

2006

European Respiratory Journal

131

118

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b 2 -Adrenoceptor agonists evoke rapid bronchodilatation and are the mainstay of the treatment of asthma symptoms worldwide. The mechanism of action of this class of compounds is believed to involve the stimulation of adenylyl cyclase and subsequent activation of the cyclic adenosine monosphosphate (cAMP)/cAMP-dependent protein kinase cascade.This classical model of b 2 -adrenoceptor-mediated signal transduction is deeply entrenched, but there is compelling evidence that agonism of b 2 -adrenoceptors can lead to the activation of multiple effector pathways, which now compels researchers in academia and the pharmaceutical industry alike to think beyond the traditional dogma. Therefore, the regulation by b 2 -adrenoceptor agonists of responses, including airways smooth muscle tone and the secretory capacity of the epithelium and pro-inflammatory/immune cells, may be highly complex, involving both cAMPdependent and -independent mechanisms that, in many cases, may act in concert.In this article, the current status of b 2 -adrenoceptor-mediated signalling in the airways is reviewed in the context of understanding mechanisms that may underlie both the beneficial and detrimental effects of these drugs in asthma symptom management.

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“…Hence, these studies show that rat thoracic aorta (with intact endothelium) possesses functional b 2 -but not b 1 -receptors. In pig basilar artery a b 1 /b 2 ratio of approximately 65:35 was found (Miyamoto et al 1993) and in endothelial cells of bovine aorta 13% of the b -adrenoceptors belong to the b 1 -subtype (Zink et al 1993). In isolated rat cerebral arteries Hempelmann and Ziegler (1993) found that the isoproterenol-induced relaxation is mediated by different b -adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

Contribution of ATP-sensitive potassium channels to β-adrenoceptor-mediated responses

Hüsken

Pfaffendorf

Zwieten

1996

Naunyn-Schmiedeberg's Arch Pharmacol

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Contribution of ATP-sensitive potassium channels to B-adrenoceptor-mediated responses Husken, B.C.P.; Pfaffendorf, M.; van Zwieten, P.A. Published in:Naunyn-Schmiedeberg's Archives of Pharmacology Link to publication Citation for published version (APA):Husken, B. C. P., Pfaffendorf, M., & van Zwieten, P. A. (1997). Contribution of ATP-sensitive potassium channels to B-adrenoceptor-mediated responses. Naunyn-Schmiedeberg's Archives of Pharmacology, 355, 97-102. General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract In isolated hearts the inotropic response to the b -adrenoceptor agonist isoproterenol is known to be abolished after ischaemia and reperfusion. The aim of this study was to investigate whether at decreased glucose levels the b -adrenoceptor-mediated responses in vascular smooth muscle would be depressed, since low glucose conditions mimick the influence of ischaemia. Accordingly, we investigated the influence of low glucose levels in the extracellular space on the vasorelaxation induced by isoproterenol and salbutamol in rat isolated thoracic aortic ring preparations with an intact endothelium and we attempted to further analyze the underlying mechanisms. Therefore, forskolin, dibutyryl-cAMP and glibenclamide (an ATP-sensitive K + -channel blocker) were studied as well.In a glucose-free medium the concentration-response curve for isoproterenol was shifted to the left compared to that obtained under normal glucose conditions. The maximal relaxation induced by isoproterenol was not affected by the absence of glucose. In contrast, the maximal relaxation induced by salbutamol in glucose-free medium decreased by 50% compared to that obtained under normal glucose conditions. Glibenclamide caused a concentrationdependent decrease of the maximum relaxation by isoproterenol in a glucose-free medium, but had no effect under normal glucose conditions. Glibenclamide did not influence the concentration-response curves for salbutamol, neither in the presence nor in the absence of glucose in the medium. The relaxation caused by forskolin and dibutyryl-cAMP was not influenced by glibenclamide in a medium devoid of glucose. In endothelium-denuded preparations glibenclamide did not affect isoproterenol-induced responses neither in the presence nor in the absence of g...

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Regulation of endothelial permeability by β-adrenoceptor agonists: Contribution of β1- and β2-adrenoceptors

Cited by 39 publications

References 41 publications

Effect of a β₂-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Effect of a β₂-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Contribution of ATP-sensitive potassium channels to β-adrenoceptor-mediated responses

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Regulation of endothelial permeability by β-adrenoceptor agonists: Contribution of β1- and β2-adrenoceptors

Cited by 39 publications

References 41 publications

Effect of a β2-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Effect of a β2-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Contribution of ATP-sensitive potassium channels to β-adrenoceptor-mediated responses

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Product

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Effect of a β₂-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction

Effect of a β₂-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction