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Endothelin-A receptors and NO mediate decrease in arterial pressure during recovery from restraint.

Avery W C Yip1, Teresa L Krukoff

  • 1Department of Cell Biology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta T6G 2H7, Canada.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|February 8, 2002
PubMed
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Central endothelin-A (ET(A)) receptors and nitric oxide (NO) influence arterial pressure during stress. Blocking ET(A) receptors increased blood pressure during stress and recovery, suggesting a role in pressure regulation.

Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Stress significantly impacts arterial pressure regulation.
  • Endothelin-A (ET(A)) receptors and nitric oxide (NO) are implicated in cardiovascular control.
  • The specific roles of central ET(A) receptors and NO in stress-induced arterial pressure changes require elucidation.

Purpose of the Study:

  • To investigate the role of central endothelin-A (ET(A)) receptors and nitric oxide (NO) in regulating arterial pressure during restraint stress and recovery.
  • To determine if blocking ET(A) receptors affects arterial pressure responses to stress.
  • To explore the involvement of NO in mediating these effects.

Main Methods:

  • Rats received intracerebroventricular (icv) injections of the ET(A) receptor antagonist BQ123.

Related Experiment Videos

  • Animals were subjected to repeated cycles of restraint stress and recovery.
  • Arterial pressure was monitored, and brainstem NO levels were assessed.
  • Nitric oxide synthase (NOS) inhibitors (L-NNA, 7-nitroindazole) were administered to assess NO's role.

    • Main Results:

    • BQ123 treatment resulted in significantly higher mean arterial pressure (MAP) during restraint and recovery compared to controls.
    • Control rats exhibited a decrease in MAP below baseline during rest periods, which was abolished by BQ123.
    • NO content in the brainstem was decreased in BQ123-treated rats.
    • NOS inhibition (L-NNA) prevented the decrease in MAP during rest periods in both groups.

    Conclusions:

    • Central ET(A) receptor activation contributes to the decrease in arterial pressure during and after restraint stress.
    • Endothelin may modulate arterial pressure during stress, potentially via the release of NO in the brainstem.
    • These findings highlight a novel pathway for cardiovascular regulation during stress.