CIRCUMSTANTIAL EVIDENCE FOR INCREASED POTASSIUM CONDUCTANCE OF MEMBRANE OF CARDIAC-MUSCLE BY 2-NICOTINAMIDOETHYL NITRATE (SG-75)

被引:65
作者
YANAGISAWA, T
SATOH, K
TAIRA, N
机构
[1] Department of Pharmacology, Tohoku University School of Medicine
关键词
D O I
10.1254/jjp.29.687
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The mechanism of action of 2-nicotinamidoethyl nitrate (SG-75), was investigated by the use of arterially blood-perfused papillary muscle preparations of the dog. All drugs were administered intra-arterially. SG-75 shortened the effective refractory period (ERP) and decreased the rate of automaticity and developed tension of the papillary muscle, whereas verapamil failed to change the ERP despite a decrease in the developed tension. SG-75 in extremely high doses induced ventricular fibrillation. Methacholine produced decreases in the rate of automaticity and developed tension, and the actions were abolished by atropine. The SG-75-induced decreases in two parameters were not modified by atropine. These results indicate that the cardiac action of SG-75 differs from that of calcium-antagonistic vasodilators and it is suggested that the basic mechanism of action of SG-75 involves an increase in potassium con ductance in the membrane of cardiac muscle, without mediation through muscarinic receptors. © 1979, The Japanese Pharmacological Society. All rights reserved.
引用
收藏
页码:687 / 694
页数:8
相关论文
共 19 条
[1]  
Uchida Y., Yoshimoto N., Murao S., Effect of 2-nicotinamidethyl nitrate (SG-75) on coronary circulation, Japan. Heart J., 19, pp. 112-124, (1978)
[2]  
Taira N., Satoh K., Yanagisawa T., Imai Y., Hiwatari M., Pharmacological profile of a new coronary vasodilator drug, 2-nicotinamidoethyl nitrate (SG-75), Clin. exp. Pharmacol. Physiol., 6, pp. 301-315, (1979)
[3]  
Fleckenstein A., Specific pharmacology of calcium in myocardium, cardiac pacemakers, and vascular smooth muscle, A. Rev. Pharmacol., 17, pp. 149-166, (1977)
[4]  
Charlier R., Nitrates. Antianginal drugs. Pathophysiological, haemodynamic, methodological, pharmacological, biochemical and clinical basis for their use in human therapeutics, Handbook of Experimental Pharmacology, 31, pp. 118-150, (1971)
[5]  
Endoh M., Hashimoto K., Pharmacological evidence of autonomic nerve activities in canine papillary muscle, Am. J. Physiol., 218, pp. 1459-1463, (1970)
[6]  
Taira N., Iijima T., Narimatsu A., Satoh K., Yanagisawa T., Effects on atrioventricular conduction of propranolol, pindolol and carteolol in the dog heart in situ as assessed by automated devices, Japan. J. Pharmacol., 28, pp. 473-483, (1978)
[7]  
Fleckenstein A., Specific inhibitors and promoters of calcium action in the excitation contraction coupling of heart muscle and their role in the prevention or production of myocardial lesions, Calcium and the Heart, pp. 135-188, (1971)
[8]  
Narimatsu A., Taira N., Effects on atrio-ventricular conduction of calcium-antago-nistic coronary vasodilators, local anaesthetics and quinidine injected into the posterior and the anterior septal artery of the atrio-ventricular node preparation of the dog, Arch. Pharmacol., 294, pp. 169-177, (1976)
[9]  
Himori N., Ono H., Taira N., Simultaneous assessment of effects of coronary vaso dilators on the coronary blood flow and the myocardial contractility by using the blood-perfused canine papillary muscle, Japan. J. Pharmacol., 26, pp. 427-435, (1976)
[10]  
Rosenblueth A., The mechanism of auricular flutter and auricular fibrillation, Circulation, 7, pp. 612-613, (1953)