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- Title
Nitric oxide synthases in vagal neurons are crucial for the regulation of heart rate in awake dogs.
- Authors
Picker, Olaf; Scheeren, Thomas W. L.; Arndt, Joachim O.
- Abstract
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 of the nervous system (n-NOS). If so, heart rate variability (HRV) as a measure of vagal activity should be an indicator of the activity of n-NOS in vagal neurons. To test this, we studied the dose-effect relations of L-NAME (0.3 – 50 mg·kg-1) on heart rate (HR), HRV and systemic vascular resistance (SVR) in seven awake dogs. HRV was analyzed in the time domain as standard deviation of the RR-intervals (SDNN) and in the frequency domain as power in the high (0.15 – 0.5 Hz) and low (0.04 – 0.15 Hz) frequency range. The effects of HR and SDNN reached their maxima at a dose of 3 mg·kg-1 and had their ED50 at 0.27 ± 0.03 mg·kg-1 and 0.43 ± 0.1 mg·kg-1, respectively, whereas SVR had its maximum at 10 mg·kg-1 and ED50 at 0.86 ± 0.11 mg·kg-1 (p < 0.05). HF-power (vagal activity) predominated compared to LF-power (mainly sympathetic activity) during baseline as well as after L-NAME. The effects on HR and HRV were absent after ganglionic blockade (hexamethonium), whereas the effects on SVR remained unchanged. Thus, NO exerts a powerful restraining activity on vagal neurons and plays a key role in the adjustment of heart rate in awake resting animals with prevailing vagal activity.
- Subjects
NEURONS; NITRIC oxide; ENDOTHELIUM; NERVOUS system; HEART beat; BRADYCARDIA
- Publication
Basic Research in Cardiology, 2001, Vol 96, Issue 4, p395
- ISSN
0300-8428
- Publication type
Article
- DOI
10.1007/s003950170048