R Busse

Summary

Affiliation: Johann Wolfgang Goethe University
Country: Germany

Publications

  1. ncbi request reprint Endothelial dysfunction coincides with an enhanced nitric oxide synthase expression and superoxide anion production
    A Bouloumie
    Zentrum der Physiologie, Klinikum der J W Goethe Universitat, Frankfurt Main, Germany
    Hypertension 30:934-41. 1997
  2. ncbi request reprint Endothelium-derived hyperpolarizing factor, but not nitric oxide, is reversibly inhibited by brefeldin A
    J Bauersachs
    Institut für Kardiovaskuläre Physiologie, Zentrum der Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Hypertension 30:1598-605. 1997
  3. ncbi request reprint The coronary endothelium-derived hyperpolarizing factor (EDHF) stimulates multiple signalling pathways and proliferation in vascular cells
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Pflugers Arch 442:511-8. 2001
  4. ncbi request reprint Ca2+-independent activation of the endothelial nitric oxide synthase in response to tyrosine phosphatase inhibitors and fluid shear stress
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Circ Res 82:686-95. 1998
  5. ncbi request reprint Increased nitrovasodilator sensitivity in endothelial nitric oxide synthase knockout mice: role of soluble guanylyl cyclase
    R P Brandes
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt, Germany
    Hypertension 35:231-6. 2000
  6. pmc Isometric contraction induces the Ca2+-independent activation of the endothelial nitric oxide synthase
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Theodor Stern Kai 7, D 60590 Frankfurt am Main, Germany
    Proc Natl Acad Sci U S A 96:1123-8. 1999
  7. ncbi request reprint Hyperthyroidism enhances endothelium-dependent relaxation in the rat renal artery
    E Büssemaker
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Theodor Stern Kai 7, D 60596 Frankfurt am Main, Germany
    Cardiovasc Res 59:181-8. 2003
  8. pmc Inhibition of the production of endothelium-derived hyperpolarizing factor by cannabinoid receptor agonists
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Br J Pharmacol 126:949-60. 1999
  9. ncbi request reprint Thrombin activates the hypoxia-inducible factor-1 signaling pathway in vascular smooth muscle cells: Role of the p22(phox)-containing NADPH oxidase
    A Gorlach
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt M, Germany
    Circ Res 89:47-54. 2001
  10. ncbi request reprint Oxidative stress and expression of p22phox are involved in the up-regulation of tissue factor in vascular smooth muscle cells in response to activated platelets
    A Gorlach
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, 60590 Frankfurt Main, Germany
    FASEB J 14:1518-28. 2000

Detail Information

Publications24

  1. ncbi request reprint Endothelial dysfunction coincides with an enhanced nitric oxide synthase expression and superoxide anion production
    A Bouloumie
    Zentrum der Physiologie, Klinikum der J W Goethe Universitat, Frankfurt Main, Germany
    Hypertension 30:934-41. 1997
    ..This would suggest that the development of endothelial dysfunction is linked to an overproduction of not one, but two, endothelium-derived radicals that might lead to the formation of peroxynitrite...
  2. ncbi request reprint Endothelium-derived hyperpolarizing factor, but not nitric oxide, is reversibly inhibited by brefeldin A
    J Bauersachs
    Institut für Kardiovaskuläre Physiologie, Zentrum der Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Hypertension 30:1598-605. 1997
    ....
  3. ncbi request reprint The coronary endothelium-derived hyperpolarizing factor (EDHF) stimulates multiple signalling pathways and proliferation in vascular cells
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Pflugers Arch 442:511-8. 2001
    ..These observations indicate that EDHF/11,12-EET is not simply a vasodilator and that its continuous release under pulsatile conditions in vivo may affect vascular cell signalling and proliferation...
  4. ncbi request reprint Ca2+-independent activation of the endothelial nitric oxide synthase in response to tyrosine phosphatase inhibitors and fluid shear stress
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Circ Res 82:686-95. 1998
    ....
  5. ncbi request reprint Increased nitrovasodilator sensitivity in endothelial nitric oxide synthase knockout mice: role of soluble guanylyl cyclase
    R P Brandes
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt, Germany
    Hypertension 35:231-6. 2000
    ..Both the acute cessation of endothelial NO formation in WT mice and the chronic deficiency of NO in eNOS(-/-) mice restore the NO sensitivity of sGC and enhance vascular smooth muscle relaxation in response to nitrovasodilator agents...
  6. pmc Isometric contraction induces the Ca2+-independent activation of the endothelial nitric oxide synthase
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Theodor Stern Kai 7, D 60590 Frankfurt am Main, Germany
    Proc Natl Acad Sci U S A 96:1123-8. 1999
    ..Thus, isometric contraction activates eNOS via a Ca2+-independent, tyrosine kinase inhibitor-sensitive pathway and, like shear stress, seems to be an independent determinant of mechanically induced NO formation...
  7. ncbi request reprint Hyperthyroidism enhances endothelium-dependent relaxation in the rat renal artery
    E Büssemaker
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Theodor Stern Kai 7, D 60596 Frankfurt am Main, Germany
    Cardiovasc Res 59:181-8. 2003
    ..Hyperthyroidism has pronounced effects on vascular function and endothelium-dependent relaxation. The aim of the present study was to identify mechanisms underlying hyperthyroidism-induced alterations in endothelial function in rats...
  8. pmc Inhibition of the production of endothelium-derived hyperpolarizing factor by cannabinoid receptor agonists
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Br J Pharmacol 126:949-60. 1999
    ..5. These results suggest that the activation of endothelial CB1 receptors appears to be negatively coupled to the production of EDHF...
  9. ncbi request reprint Thrombin activates the hypoxia-inducible factor-1 signaling pathway in vascular smooth muscle cells: Role of the p22(phox)-containing NADPH oxidase
    A Gorlach
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt M, Germany
    Circ Res 89:47-54. 2001
    ....
  10. ncbi request reprint Oxidative stress and expression of p22phox are involved in the up-regulation of tissue factor in vascular smooth muscle cells in response to activated platelets
    A Gorlach
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, 60590 Frankfurt Main, Germany
    FASEB J 14:1518-28. 2000
    ..These results indicate that activated platelets up-regulate TF expression and that this response involves ROS generation and a p22phox-containing NAD(P)H oxidase in SMC...
  11. ncbi request reprint gp91phox-containing NADPH oxidase mediates endothelial dysfunction in renovascular hypertension
    O Jung
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Circulation 109:1795-801. 2004
    ..We hypothesized that the endothelial gp91phox-containing NADPH oxidase is predominant in generating the O2- to scavenge endothelial NO and thus is responsible for the development of endothelial dysfunction...
  12. ncbi request reprint Vascular endothelial growth factor up-regulates nitric oxide synthase expression in endothelial cells
    A Bouloumie
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Cardiovasc Res 41:773-80. 1999
    ....
  13. ncbi request reprint Calcium signalling and autacoid production in endothelial cells are modulated by changes in tyrosine kinase and phosphatase activity
    I Fleming
    Zentrum der Physiologie, Klinikum der J W Goethe Universitat, Frankfurt Main, Germany
    J Vasc Res 33:225-34. 1996
    ..These observations suggest that alterations in cellular levels of phosphotyrosine may have profound effects on vascular homeostasis by modulating Ca2+ signalling and autacoid production in endothelial cells...
  14. ncbi request reprint Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance
    R Popp
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Franfurt, Germany
    Circ Res 82:696-703. 1998
    ....
  15. ncbi request reprint A gp91phox containing NADPH oxidase selectively expressed in endothelial cells is a major source of oxygen radical generation in the arterial wall
    A Gorlach
    Institut für Kardiovaskuläre Physiologie, Institut für Anatomie II F D, Klinikum der J W Goethe Universitat, Frankfurt Main, Germany
    Circ Res 87:26-32. 2000
    ..These data demonstrate that ECs, in contrast to SMCs, express a gp91phox-containing leukocyte-type NADPH oxidase. This enzyme is a major source for arterial ROS generation and affects the bioavailability of endothelium-derived NO...
  16. ncbi request reprint Leptin induces oxidative stress in human endothelial cells
    A Bouloumie
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt Main, Germany
    FASEB J 13:1231-8. 1999
    ..Thus, chronic oxidative stress in endothelial cells under hyperleptinemia may activate atherogenic processes and contribute to the development of vascular pathology...
  17. ncbi request reprint Signal transduction of eNOS activation
    I Fleming
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Cardiovasc Res 43:532-41. 1999
    ....
  18. ncbi request reprint Calcium-dependent and calcium-independent activation of the endothelial NO synthase
    I Fleming
    Zentrum der Physiologie, Klinikum der J W Goethe Universitat, Frankfurt Main, Deutschland
    J Vasc Res 34:165-74. 1997
    ..Thus in a departure from widely held beliefs, we propose that the endothelial cells are able to respond to mechanical and humoral stimuli activating NOS III by at least two separate pathways...
  19. ncbi request reprint Thrombin-induced MCP-1 expression involves activation of the p22phox-containing NADPH oxidase in human vascular smooth muscle cells
    R P Brandes
    Institut für Kardiovaskuläre Physiologie, Klinikum der JW Goethe Universität, Frankfurt Main, Germany
    Thromb Haemost 85:1104-10. 2001
    ..Inhibition of p38 MAP kinase diminished the thrombin-induced expression of MCP-1...
  20. pmc An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice
    R P Brandes
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt am Main, Germany
    Proc Natl Acad Sci U S A 97:9747-52. 2000
    ....
  21. pmc The extracellular regulated kinases (ERK) 1/2 mediate cannabinoid-induced inhibition of gap junctional communication in endothelial cells
    R P Brandes
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Theodor Stern Kai 7, 60596 Frankfurt am Main, Germany
    Br J Pharmacol 136:709-16. 2002
    ..Moreover, the activation of ERK1/2 by endothelial cell agonists such as bradykinin, appears to exert a negative feedback inhibition on EDHF-mediated responses...
  22. ncbi request reprint Withdrawal of cerivastatin induces monocyte chemoattractant protein 1 and tissue factor expression in cultured vascular smooth muscle cells
    R P Brandes
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Theodor Stern Kai 7, D 60596 Frankfurt am Main, Germany
    Arterioscler Thromb Vasc Biol 23:1794-800. 2003
    ..We determined in vascular smooth muscle cells whether statin withdrawal leads to the expression of proinflammatory genes involved in the development and progression of arteriosclerosis...
  23. pmc Potentiation by ACE inhibitors of the dilator response to bradykinin in the coronary microcirculation: interaction at the receptor level
    M Hecker
    Center of Physiology, JWG University Clinic, Frankfurt Main, Germany
    Br J Pharmacol 111:238-44. 1994
    ....
  24. ncbi request reprint Leptin, the product of Ob gene, promotes angiogenesis
    A Bouloumie
    Institut für Kardiovaskuläre Physiologie, Klinikum der J W Goethe Universitat, Frankfurt Main, Germany
    Circ Res 83:1059-66. 1998
    ....