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Nitric oxide mediates capsaicin-induced increase in cochlear blood flow
Z Vass1, P B Brechtelsbauer, A L Nuttall
1Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor 48109-0506, USA.
Hearing Research
|October 1, 1996
Summary
This study reveals that nitric oxide (NO) mediates capsaicin-induced increases in cochlear blood flow (CBF). Inhibiting NO significantly reduces the vasodilatory effects of capsaicin on the cochlea.
Area of Science:
- Oto-neuroscience
- Vascular physiology
- Pharmacology
Background:
- Capsaicin is known to elevate cochlear blood flow (CBF) in a dose-dependent manner.
- The precise mechanisms, particularly the role of nitric oxide (NO), in capsaicin's effect on CBF require further elucidation.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in mediating capsaicin-induced changes in cochlear blood flow (CBF).
Main Methods:
- Utilized laser Doppler flowmetry in anesthetized guinea pigs.
- Administered capsaicin to the round window membrane (RWM) before and after inhibiting NO synthase with NG-nitro-L-arginine methyl ester (L-NAME).
Main Results:
- Capsaicin administration significantly increased CBF.
- Inhibition of NO synthase with L-NAME (intravenously or topically) markedly attenuated the capsaicin-induced increase in CBF.
- These findings suggest NO is a key mediator in capsaicin's vasodilatory effects on cochlear vasculature.
Conclusions:
- Nitric oxide (NO) plays a crucial role as a mediator in the regulation of cochlear blood flow (CBF) by capsaicin-sensitive sensory neurons.
- The study supports a pathway where capsaicin stimulates sensory neurons, leading to NO release and subsequent vasodilation in the cochlea.