Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, Osaka 565-8565, Japan.
Department of Cardiac Physiology, National Cerebral and Cardiovascular Center, Osaka 565-8565, Japan.
Auton Neurosci. 2019 May;218:25-30. doi: 10.1016/j.autneu.2019.02.005. Epub 2019 Feb 18.
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.
已知交感神经和副交感神经对心脏的控制之间存在复杂的相互作用。虽然交感神经刺激(SNS)通常会增强迷走神经刺激(VNS)对心率(HR)的反应,但外源性给予去甲肾上腺素(NE)也可以减弱 HR 的反应以及 VNS 期间心肌间质乙酰胆碱(ACh)的释放。为了提供一个关于交感神经对迷走神经控制心脏的拮抗作用的综合知识基础,我们研究了 SNS 是否会显著减弱体内跳动心脏中 VNS 诱导的心肌间质 ACh 释放。在九只麻醉大鼠中,在没有和存在 5 Hz 背景 SNS 的情况下,检查了 HR 和心肌间质 ACh 释放对 5 Hz 和 20 Hz VNS 的变化。SNS 显著增强了 20 Hz VNS 期间的 VNS 诱导的 HR 降低(-101.2 ± 33.1 与-163.0 ± 34.9 次/分钟,P < 0.001,增强 60%)。相比之下,SNS 显著减弱了 20 Hz VNS 期间的 ACh 释放(4.30 ± 0.72 与 3.80 ± 0.75 nM,P < 0.01,衰减 12%)。总之,SNS 仅对体内跳动心脏中 VNS 诱导的心肌间质 ACh 释放产生适度的抑制作用。