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Related Experiment Videos

ATP-induced cochlear blood flow changes involve the nitric oxide pathway

T Ren1, A L Nuttall, J M Miller

  • 1Oregon Hearing Research Center, Oregon Health Sciences University, Portland 97201-3098, USA. rent@ohsu.edu

Hearing Research
|November 21, 1997
PubMed
Summary

Adenosine triphosphate (ATP) influences cochlear blood flow (CBF) by causing dose-dependent increases, potentially mediated by nitric oxide pathways and purinoceptors. This study reveals ATP

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Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Otolaryngology

Background:

  • Cochlear blood flow (CBF) regulation is crucial for hearing function.
  • Mechanisms controlling CBF are not fully understood, particularly the role of adenosine triphosphate (ATP).
  • ATP is a known vasoactive agent in other organ systems.

Purpose of the Study:

  • To investigate the effects of ATP on CBF in guinea pigs.
  • To determine if the nitric oxide (NO) pathway is involved in ATP-induced CBF changes.
  • To explore the purinoceptor subtypes mediating these responses.

Main Methods:

  • Anesthetized guinea pigs were used with exposed anterior inferior cerebellar artery (AICA).
  • ATP was perfused into the AICA, and CBF was measured using laser Doppler flowmetry.

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  • The role of the nitric oxide pathway was assessed using N(omega)-nitro-L-arginine methyl ester (L-NAME).
  • Main Results:

    • ATP perfusion induced dose-dependent increases in CBF, reaching up to 220% of baseline.
    • A biphasic response (transient decrease followed by increase) was observed in some animals.
    • L-NAME attenuated ATP-induced CBF increases and enhanced decreases, suggesting NO pathway involvement.
    • Sodium nitroprusside (SNP)-induced CBF changes were unaffected by L-NAME.

    Conclusions:

    • ATP plays a significant role in regulating cochlear blood flow.
    • The biphasic CBF response suggests involvement of both P2x and P2y purinoceptors.
    • ATP-induced increases in CBF are likely mediated by nitric oxide release via endothelial P2y-purinoceptor activation.