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Arterial baroreflex dysfunction impairs ischemia-induced angiogenesis.

Changning Hao1, Zhen-Hao Huang, Shu-Wei Song

  • 1Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Journal of the American Heart Association
|May 14, 2014
PubMed
Summary

Arterial baroreflex dysfunction impairs blood vessel growth after limb ischemia by reducing endothelium-derived acetylcholine signaling. Restoring this signaling pathway with pyridostigmine improves angiogenesis.

Keywords:
acetylcholinesterase inhibitorangiogenesisarterial baroreflexnon‐neural cholinergic systemperipheral vascular disease

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Area of Science:

  • Cardiovascular Physiology
  • Vascular Biology
  • Regenerative Medicine

Background:

  • Endothelium-derived acetylcholine (eACh) regulates vascular responses to hypoxia.
  • Arterial baroreflex (ABR) dysfunction compromises the eACh system.
  • Investigating ABR dysfunction's impact on ischemia-induced angiogenesis is crucial.

Purpose of the Study:

  • To determine the effect of ABR dysfunction on ischemia-induced angiogenesis.
  • To elucidate the role of eACh/nicotinic acetylcholine receptor (nAChR) signaling in this process.

Main Methods:

  • Hindlimb ischemia model in rats with induced ABR dysfunction (sinoaortic denervation - SAD).
  • Treatment with acetylcholinesterase inhibitor (pyridostigmine) in SAD rats.
  • Assessment of angiogenic parameters and molecular factors (VEGF, HIF-1α).
  • Experiments in α7-nAChR knockout mice and use of nicotinic receptor blockers.

Main Results:

  • SAD rats showed impaired angiogenesis (reduced skin temperature, capillary density) and lower VEGF/HIF-1α levels.
  • Pyridostigmine treatment restored angiogenic action and eACh levels in SAD rats.
  • Pyridostigmine improved angiogenesis and VEGF/HIF-1α levels in α7-nAChR knockout mice.
  • Nicotinic receptor blockade inhibited ACh-induced VEGF expression and VEGFR2 phosphorylation.

Conclusions:

  • ABR dysfunction impairs ischemia-induced angiogenesis.
  • This impairment is mediated by reduced eACh/α7-nAChR-dependent and -independent HIF-1α/VEGF-VEGFR2 signaling.
  • Targeting the eACh system may offer therapeutic potential for ischemic conditions.