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Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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[Vasopressin and angiogenesis].

Gérard Alonso1

  • 1UMR CNRS 5203, Institut de Génomique Fonctionnelle, 34000 Montpellier, France.

Journal De La Societe De Biologie
|April 11, 2009
PubMed
Summary

Osmotic stimulation triggers angiogenesis in the brain's magnocellular nuclei. This process involves hypoxia and is mediated by arginine vasopressin (AVP) acting on V1a receptors, constricting local arterioles.

Area of Science:

  • Neuroscience
  • Physiology
  • Vascular Biology

Background:

  • Central nervous system (CNS) vasculature is typically quiescent in adults.
  • Previous studies suggested astrocyte and endothelial cell proliferation in hypothalamic magnocellular nuclei during hyperosmotic stimulation.

Purpose of the Study:

  • To investigate the mechanisms of angiogenesis in hypothalamic magnocellular nuclei induced by osmotic stimulation.
  • To elucidate the role of vascular endothelial growth factor (VEGF) and arginine vasopressin (AVP) in this process.

Main Methods:

  • Utilized advanced techniques to study cellular proliferation and angiogenesis.
  • Measured VEGF expression and local hypoxia.
  • Employed Brattleboro rats (AVP-deficient) and Wistar rats.

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  • Investigated the effects of AVP infusion, V1a receptor (V1a-R) stimulation, and V1a-R antagonist administration.

    • Main Results:

    • Osmotic stimulus primarily induces local angiogenesis, not just cell proliferation.
    • Hypothalamic neurons express VEGF, crucial for osmotic-induced angiogenesis.
    • Angiogenesis correlates with increased VEGF and local hypoxia.
    • AVP is essential; its absence prevents hypoxia and angiogenesis.
    • AVP constricts afferent arterioles via V1a-R, causing hypoxia and subsequent angiogenesis.

    Conclusions:

    • Osmotic stimulation induces hypothalamic angiogenesis via hypoxia.
    • AVP-mediated constriction of arterioles through V1a-R stimulation is the key mechanism.
    • Local AVP release from dendrites triggers V1a-R, leading to hypoxia and angiogenesis.