Highlights
- •Interactions between sympathetic (SNS) and vagal nerve stimulation (VNS) in regulating the heart were examined.
- •SNS enhanced the VNS-induced heart rate response in agreement with the concept of accentuated antagonism.
- •SNS reduced the VNS-induced acetylcholine release less potently than exogenous norepinephrine.
Abstract
Complex interactions are known to occur between the sympathetic and parasympathetic
controls of the heart. Although sympathetic nerve stimulation (SNS) usually augments
the heart rate (HR) response to vagal nerve stimulation (VNS), exogenously administered
norepinephrine (NE) can attenuate the HR response as well as the myocardial interstitial
acetylcholine (ACh) release during VNS. To provide a basis for an integrative knowledge
about the opposing adrenergic effects on the vagal control of the heart, we examined
whether SNS significantly attenuates VNS-induced myocardial interstitial ACh release
in the in vivo beating heart. In nine anesthetized rats, changes in HR and myocardial
interstitial ACh release in response to 5- and 20-Hz VNS were examined in both the
absence and presence of a 5-Hz background SNS. The SNS significantly enhanced the
VNS-induced HR reduction during 20-Hz VNS (−101.2 ± 33.1 vs. –163.0 ± 34.9 beats/min,
P < 0.001, a 60% augmentation). By contrast, the SNS significantly attenuated the ACh
release during 20-Hz VNS (4.30 ± 0.72 vs. 3.80 ± 0.75 nM, P < 0.01, a 12% attenuation). In conclusion, SNS exerted only a moderate inhibitory
effect on the VNS-induced myocardial interstitial ACh release in the in vivo beating
heart.
Keywords
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Article info
Publication history
Published online: February 18, 2019
Accepted:
February 17,
2019
Received in revised form:
January 30,
2019
Received:
December 6,
2018
Identification
Copyright
© 2019 Elsevier B.V. All rights reserved.