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Does central nitric oxide elicit pulmonary hypertension in conscious rats?
Daryl O Schwenke1, James T Pearson, Hidezo Mori
1Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Osaka, Japan. schwenke@ri.ncvc.go.jp
Respiratory Physiology & Neurobiology
|January 13, 2006
Summary
Central nitric oxide (NO) may influence pulmonary arterial pressure (PAP). This study investigated NO
Area of Science:
- Cardiovascular Physiology
- Respiratory Medicine
- Neuroscience
Background:
- Pulmonary arterial hypertension (PAH) pathogenesis is not fully understood.
- Nitric oxide (NO) plays a role in regulating sympathetic outflow and may affect pulmonary arterial pressure (PAP).
Purpose of the Study:
- To investigate the role of central nitric oxide (NO) in modulating pulmonary arterial pressure (PAP), particularly during chronic hypoxia-induced pulmonary arterial hypertension (PAH).
Main Methods:
- 20 Sprague-Dawley rats were instrumented for telemetric PAP measurement and intracerebroventricular (i.c.v.) infusion of aCSF, L-NAME, or a NO-donor (SIN-1).
- Rats were exposed to normoxia followed by 14 days of chronic hypoxia (12% O2).
Main Results:
- Exogenous NO (SIN-1) increased PAP by ~64% in normoxia, an effect blocked by isoproterenol.
- Chronic hypoxia induced PAH in all rats.
- L-NAME did not affect baseline mean PAP (MPAP) or hypoxic responses.
Conclusions:
- Central NO administration elevates mean pulmonary arterial pressure (MPAP).
- The precise mechanisms by which central NO influences MPAP and PAH require further investigation.
