Antiarrhythmic effect of acupuncture pretreatment in rats subjected to simulative global ischemia and reperfusion--involvement of adenylate cyclase, protein kinase A, and L-type Ca2+ channel.
Our previous study showed that electro-acupuncture (EA) pretreatment protects the heart from injury of ischemia. The present study explored further whether adenylate cyclase (AC), protein kinase A (PKA), and L-type Ca(2+) channel, the beta(1)-AR signaling components modulating intracellular Ca(2+) ([Ca(2+)](i)), are involved in the mediation of the antiarrhythmic effect of EA pretreatment in the rats from which the hearts were subsequently isolated and subjected to simulative global ischemia and reperfusion (SGIR). SGIR was performed by perfusing the isolated heart at a low flow followed by normal perfusion. Adult rats were randomized into four groups, namely, normal control (NC), SGIR, EA, and NC plus EA (NCEA) groups. The rats in the EA and NCEA groups were given EA pretreatment at bilateral Neiguan points (PC6) for 30 min once a day in 3 consecutive days before the hearts were isolated and perfused. The arrhythmia score and the response of [Ca(2+)](i) to the activators of AC, PKA, and L-type Ca(2+) channel in single ventricular myocyte isolated from the hearts subjected to SGIR were compared among the groups. The results showed that the arrhythmia score was significantly higher in the SGIR group as compared with the NC and NCEA groups. The SGIR-enhanced arrhythmia score was significantly attenuated in the EA group. More interesting, EA pretreatment also attenuated the SGIR-enhanced response of [Ca(2+)](i) to the activators of AC, PKA, and the L-type Ca(2+) channel in the myocytes isolated from the hearts subjected to SGIR. In conclusion, EA pretreatment can produce an antiarrhythmic effect in the rat of SGIR. AC, PKA and the L-type Ca(2+) channel are involved in the mediation of the antiarrhythmic effect of EA pretreatment.
Department of Physiology, Institute of Acupuncture, China Academy of Chinese Medical Sciences, Dongzhimennei, Dongcheng District, Beijing, P R China.
Junhong
J
Gao
Ling
L
Zhang
Yumin
Y
Wang
Bo
B
Lu
Haifeng
H
Cui
Weixing
W
Fu
Hongxin
H
Wang
Youhua
Y
Yu
Xiaochun
X
Yu
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000262:Adenylyl Cyclases / Q000378:metabolism*; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000201:enzymology / Q000209:etiology / Q000517:prevention & control*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000378:metabolism*; D020013:Calcium Signaling; D005576:Colforsin / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D004195:Disease Models, Animal; D015671:Electroacupuncture; D004562:Electrocardiography; D004789:Enzyme Activation; D020536:Enzyme Activators / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000201:enzymology / Q000628:therapy*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology*; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D018342:Receptors, Adrenergic, beta-1 / Q000378:metabolism
D002120:Calcium Channel Agonists; D020746:Calcium Channels, L-Type; D020536:Enzyme Activators; D018342:Receptors, Adrenergic, beta-1; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D017868:Cyclic AMP-Dependent Protein Kinases; D000262:Adenylyl Cyclases