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首页> 外文期刊>Autonomic neuroscience: basic & clinical >Accentuated antagonism of vagal heart rate control and less potent prejunctional inhibition of vagal acetylcholine release during sympathetic nerve stimulation in the rat
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Accentuated antagonism of vagal heart rate control and less potent prejunctional inhibition of vagal acetylcholine release during sympathetic nerve stimulation in the rat

机译：剧烈对迷肠心率控制的拮抗作用以及迷重的乙酰胆碱在大鼠同情神经刺激期间的迷住前抑制

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摘要

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.
机译：已知复杂的相互作用发生在心脏的交感神经和副交感神经之间。虽然同情神经刺激（SNS）通常增强心率（HR）对迷住神经刺激（VNS）的反应，但外源给药的去甲肾上腺素（NE）可以衰减在VNS期间的HR响应以及心肌间质性乙酰胆碱（ACH）释放。为综合知识提供关于对心脏阴道控制的反对肾上腺素能作用的依据，我们检查了SNS是否显着衰减VNS诱导的体内击败心脏诱导的心肌间质性ACH释放。在九种麻醉大鼠中，在5 Hz背景SNS的缺失和存在下，检查了响应于5-和20 Hz VNS的HR和心肌间质ACH的变化。 SNS显着增强了20-Hz VNS（-101.2 +/- 33.1 Vs. -163.0 +/- 34.9节拍/ min，P <0.001，60％的增强）期间增强了VNS诱导的HR降低。相比之下，SNS在20-Hz VNS（4.30 +/- 0.72 Vs.3.80 +/- 0.75nm，P <0.01，12％衰减）中显着衰减了ACH释放。总之，SNS仅对VNS诱导的心肌内间隙ACH释放进行了适度的抑制作用。

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