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      Adrenergic Mechanism in the Control of Endothelial Function

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          Abstract

          There is considerable evidence that many disease are associated with endothelial dysfunction and reduced nitric oxide production such as hypertension, obesity, dyslipidemias, diabetes, heart failure, atherosclerosis. Notably these conditions are also characterized by alteration in the adrenergic tone. Whether these two mechanisms are just epiphenomenal each other or there is a functional link, it is still to be established. A starting ground to establish this issue is that vascular endothelium plays an important role in the function of cardiovascular system and that adrenergic receptors on endothelial cells contribute to the regulation of vasomotor tone. The aim of this excerpt is to review current knowledge on the physiology of endothelial adrenergic receptors to contribute to the basis for newer and better approaches to endothelial dysfunction in the setup of cardiovascular conditions.

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          Most cited references 75

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          The protein kinase encoded by the Akt proto-oncogene is a target of the PDGF-activated phosphatidylinositol 3-kinase.

          The serine/threonine protein kinase encoded by the Akt proto-oncogene is catalytically inactive in serum-starved primary and immortalized fibroblasts. Here we show that Akt and the Akt-related kinase AKT2 are activated by PDGF. The activation was rapid and specific, and it was abrogated by mutations in the Akt Pleckstrin homology (PH) domain. The Akt activation was also shown to depend on PDGFR beta tyrosines Y740 and Y751, which bind phosphatidylinositol 3-kinase (PI 3-kinase) upon phosphorylation. Moreover, Akt activation was blocked by the PI 3-kinase-specific inhibitor wortmannin and the dominant inhibitory N17Ras. Conversely, Akt activity was induced following the addition of phosphatidylinositol-3-phosphate to Akt immunoprecipitates from serum-starved cells in vitro. These results identify Akt as a novel target of PI 3-kinase and suggest that the Akt PH domain may be a mediator of PI 3-kinase signaling.
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            Nitric oxide synthases: roles, tolls, and controls.

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              Mechanisms of normal and tumor-derived angiogenesis.

              Often those diseases most evasive to therapeutic intervention usurp the human body's own cellular machinery or deregulate normal physiological processes for propagation. Tumor-induced angiogenesis is a pathological condition that results from aberrant deployment of normal angiogenesis, an essential process in which the vascular tree is remodeled by the growth of new capillaries from preexisting vessels. Normal angiogenesis ensures that developing or healing tissues receive an adequate supply of nutrients. Within the confines of a tumor, the availability of nutrients is limited by competition among actively proliferating cells, and diffusion of metabolites is impeded by high interstitial pressure (Jain RK. Cancer Res 47: 3039-3051, 1987). As a result, tumor cells induce the formation of a new blood supply from the preexisting vasculature, and this affords tumor cells the ability to survive and propagate in a hostile environment. Because both normal and tumor-induced neovascularization fulfill the essential role of satisfying the metabolic demands of a tissue, the mechanisms by which cancer cells stimulate pathological neovascularization mimic those utilized by normal cells to foster physiological angiogenesis. This review investigates mechanisms of tumor-induced angiogenesis. The strategies used by cancer cells to develop their own blood supply are discussed in relation to those employed by normal cells during physiological angiogenesis. With an understanding of blood vessel growth in both normal and abnormal settings, we are better suited to design effective therapeutics for cancer.
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                Author and article information

                Journal
                Transl Med UniSa
                Transl Med UniSa
                Translational Medicine @ UniSa
                Università di Salerno
                2239-9747
                2239-9747
                17 October 2011
                Sep-Dec 2011
                : 1
                : 213-228
                Affiliations
                [1 ]Department of Internal Medicine of Federico II University of Naples, Napoli, Italy
                [2 ]School of Medicine of University of Salerno, Baronissi (SA), Italy
                Author notes
                Addresses for Correspondence: Corresponding author, Daniela Sorriento, PhD, Università degli Studi di Napoli “Federico II”, Via Pansini 5, 80131 Napoli, Italia, Tel: 0817462220, Fax: 0817462256, Email: danisor@ 123456libero.it
                Senior author, Guido Iaccarino, MD, PhD, Università di Salerno, Via Salvador Allende, 84081 Baronissi (SA), Italia, Tel: 089965021, E-mail: giaccarino@ 123456unisa.it
                Article
                tm-01-13
                3728849
                23905034
                82b4826e-39e4-438e-a820-4e02a195bd2c

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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