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Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
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Lead toxicity promotes autonomic dysfunction with increased chemoreceptor sensitivity.

Vera Geraldes1, Mafalda Carvalho2, Nataniel Goncalves-Rosa1

  • 1Institute of Physiology, Faculty of Medicine of the University of Lisbon, Av. Prof Egas Moniz, 1649-028 Lisbon, Portugal; Cardiovascular Centre of the University of Lisbon, Av. Prof Egas Moniz, 1649-028 Lisbon, Portugal.

Neurotoxicology
|May 3, 2016
PubMed
Summary
This summary is machine-generated.

Lead exposure impairs autonomic nervous system function, causing hypertension and increased chemosensitivity. Angiotensin (1-7) in the NTS is implicated in this toxicity, offering potential therapeutic targets for lead poisoning.

Keywords:
A-779Baroreceptor reflexChemoreceptor reflexHypertensionLead toxicityPVN-NTS axisSympathoexcitation

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Area of Science:

  • Environmental toxicology
  • Neuroscience
  • Occupational health

Background:

  • Lead is a ubiquitous environmental toxicant with no known physiological role.
  • Occupational exposure to lead can lead to significant health issues, including autonomic nervous system dysfunction.
  • Previous studies suggest lead toxicity affects cardiorespiratory control, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate the role of the angiotensinogenic PVN-NTS axis in lead-induced autonomic dysfunction.
  • To elucidate the interplay between baroreceptor and chemoreceptor reflexes in chronic lead exposure.
  • To evaluate the effects of central angiotensin inhibition on cardiorespiratory parameters in lead-exposed rats.

Main Methods:

  • In vivo assessment of arterial pressure, heart rate, and respiratory rate in rats chronically exposed to lead.
  • Evaluation of sympathetic and parasympathetic activity, and baro- and chemoreceptor reflex profiles.
  • Administration of A-779 (angiotensin (1-7) antagonist) into the NTS to assess its effects on autonomic function.

Main Results:

  • Lead exposure resulted in increased chemosensitivity, baroreceptor reflex impairment, sympathetic over-excitation, hypertension, and tachypnea.
  • NTS treatment with A-779 reversed chemosensitivity and sympathetic over-excitation towards normal levels.
  • No significant changes in parasympathetic activity were observed before or after A-779 treatment.

Conclusions:

  • Angiotensin (1-7) acting at the NTS level plays a crucial role in the autonomic dysfunction associated with lead toxicity.
  • Increased chemosensitivity and sympathetic over-excitation indicate impaired autonomic outflow to cardiovascular and respiratory systems due to chronic lead exposure.
  • This study provides novel insights into the central mechanisms of lead-induced autonomic dysfunction, suggesting potential therapeutic strategies for lead toxicity symptoms.