Nitric oxide synthases in vagal neurons are crucial for the regulation of heart rate in awake dogs

摘要: Nitric oxide synthase (NOS) inhibitors elicit bradycardias independent of the endothelium (e-NOS) or increases in blood pressure. Therefore, this bradycardia could be mediated by other NOS isoforms, most likely that nervous system (n-NOS). If so, heart rate variability (HRV) as a measure vagal activity should an indicator n-NOS neurons. To test this, we studied dose-effect relations L-NAME (0.3 – 50 mg·kg−1) on (HR), HRV and systemic vascular resistance (SVR) seven awake dogs. was analyzed time domain standard deviation RR-intervals (SDNN) frequency power high (0.15 0.5 Hz) low (0.04 0.15 range. The effects HR SDNN reached their maxima at dose 3 mg·kg−1 had ED50 0.27 ± 0.03 0.43 0.1 mg·kg−1, respectively, whereas SVR its maximum 10 0.86 0.11 (p < 0.05). HF-power (vagal activity) predominated compared to LF-power (mainly sympathetic during baseline well after L-NAME. were absent ganglionic blockade (hexamethonium), remained unchanged. Thus, NO exerts powerful restraining neurons plays key role adjustment resting animals with prevailing activity.