[Vagal control of cardiac functions and vagal protection of ischemic myocardium].
The physiological activities of the cardiovascular system are under the control of autonomic nervous system (ANS). Recent researches have found that autonomic dysfunction, especially the withdrawal of vagal activity, was closely related to the etiology, course and prognosis of cardiovascular disease (CVD). Based on the current status and our achievements in this area, we discuss vagal regulation of different parts of the heart and the mechanism of vagal protection of myocardium. Using a force transducer and standard microelectrodes recording technology, we found that the vagus nerve transmitter--acetylcholine (ACh) had direct effects on ventricular myocytes in mammals: It inhibited the contractility and shortened the action potential duration of cardiac myocytes. We proved the existence of muscarinic receptors and vagal nerves innervation in ventricle with histochemical staining and molecular biological methods. Furthermore, ACh-activated potassium channel (KACh) was found in the ventricles of some animals by patch-clamp. Fade of the current (IK.ACh) to ACh in atrium was found in previous research, which was related to the muscarinic receptors and phosphorylation of G protein or potassium channel. However, the mechanism of the fade in ventricle needs to be further investigated. Combined with autonomic nervous evaluation methods (heart rate variability analysis) and relevant animal models, we studied the regulation of ANS during normal and morbid state, and proved the age-associated changes and compensatory effects of vagal control of hemodynamics after unilateral vagotomy. By increasing the vagal tension (ACh induced-preconditioning/postconditioning, aerobic exercise, beta receptor antagonist), we demonstrated protective effects of the vagus nerve on the ischemic myocardium and mechanism of the cholinergic anti-inflammatory effects on the inflammatory reaction induced by reperfusion injury. Evaluating cardiac autonomic nervous regulation and improving balance between sympathetic and vagal nerve will provide an important basis for the prevention and treatment of CVD.
Zang
Wei-Jin
WJ
Division of Cardiovascular Physiology and Pharmacology, Department of Pharmacology, School of Medicine, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an Jiaotong University, Xi'an 710061, China. zwj@mail.xjtu.edu.cn
Sun
Lei
L
Yu
Xiao-Jiang
XJ
Lv
Jun
J
Chen
Li-Na
LN
Liu
Bing-Hang
BH
D000109:Acetylcholine / Q000502:physiology*; D000200:Action Potentials; D000818:Animals; D001341:Autonomic Nervous System; D006339:Heart Rate; D006352:Heart Ventricles / Q000166:cytology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000502:physiology*; D015221:Potassium Channels / Q000378:metabolism; D011976:Receptors, Muscarinic / Q000378:metabolism; D014630:Vagus Nerve / Q000502:physiology*
D015221:Potassium Channels; D011976:Receptors, Muscarinic; D000109:Acetylcholine