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Does central nitric oxide chronically modulate the acute hypoxic ventilatory response in conscious rats?
D O Schwenke1, J T Pearson, K Kangawa
1Department of Biochemistry, National Cardiovascular Center Research Institute, Suita, Osaka, Japan. schwenke@ri.ncvc.go.jp
Acta Physiologica (Oxford, England)
|April 26, 2006
Summary
Long-term central nitric oxide (NO) imbalances did not alter the hypoxic ventilatory response (HVR) in rats exposed to chronic hypoxia. However, NO plays a role in HVR following chronic hypoxia exposure.
Area of Science:
- Physiology
- Neuroscience
- Respiratory Medicine
Background:
- Hypoxia triggers increased ventilation (VE) via complex pathways.
- Central nitric oxide (NO) is a key neuromodulator in this response.
- The long-term effects of central NO pathway disturbances on the hypoxic ventilatory response (HVR) remain unclear.
Purpose of the Study:
- To investigate the long-term role of central NO in modulating the HVR.
- To determine if chronic hypoxia (CH) alters the HVR through central NO pathways.
Main Methods:
- Rats received continuous intracerebroventricular infusions of artificial cerebrospinal fluid (control), L-NAME (NO synthesis inhibitor), or SIN-1 (NO donor).
- VE response to acute hypoxia was measured before and after 14 days of chronic hypoxia (12% O2).
Main Results:
- One week of central L-NAME or SIN-1 infusion did not alter the HVR magnitude.
- Chronic hypoxia did not change the HVR.
- During CH, L-NAME reduced baseline VE and HVR, affecting the frequency component.
Conclusions:
- Long-term central NO alterations do not appear to modify the HVR under moderate chronic hypoxia, likely due to compensatory mechanisms.
- Nitric oxide is implicated as an important modulator of the HVR after chronic hypoxia exposure.
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