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Nitric oxide and ventilatory response to hypoxia
M A Haxhiu1, C H Chang, I A Dreshaj
1Department of Medicine, School of Medicine Case Western Reserve University, Cleveland, OH 44106, USA.
Respiration Physiology
|September 1, 1995
Summary
Hypoxia activates the nitric oxide (NO) pathway in the brainstem, influencing respiratory responses to oxygen deprivation. This NO-cGMP signaling contributes to breathing regulation during hypoxia.
Area of Science:
- Neuroscience
- Respiratory Physiology
Background:
- Hypoxia triggers neurotransmitter release in the CNS, affecting breathing.
- Nitric oxide (NO) is increasingly recognized as a neurotransmitter in the CNS.
Purpose of the Study:
- To investigate the localization of nitric oxide synthase (NOS) in the nucleus tractus solitarius.
- To determine the role of the NO-cGMP pathway in the respiratory response to oxygen deprivation.
Main Methods:
- NADPH-diaphorase histochemistry to identify NOS-expressing neurons.
- Administration of NOS inhibitor N-omega-nitro-L-arginine to assess NO's role.
- Measurement of ventilatory and phrenic nerve responses to hypoxia in rats and cats.
Main Results:
- NOS-containing neurons were found in nucleus tractus solitarius subnuclei receiving chemoreceptor input.
- NOS inhibition attenuated the ventilatory response to hypoxia and altered phrenic nerve activity.
- NOS inhibition in sinoaortic denervated cats potentiated the decline in phrenic nerve output.
Conclusions:
- Oxygen deprivation activates the central NO-cGMP pathway, contributing to hypoxia-induced respiratory increases.
- NO may inhibit CNS hypoxia-triggered inhibitory synaptic transmission independently of peripheral chemoreceptors.