Regulation of myocardial cyclic AMP by isoproterenol, glucagon and acetylcholine |
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| Authors: | T P Lee J F Kuo P Greengard |
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| Affiliation: | 1. Department of Pharmacology, School of Medicine, Bushehr University of Medical Sciences, Iran;2. Education Development Center, Bushehr University of Medical Sciences, Iran;3. Department of Toxicology–Pharmacology, School of Pharmacy, Tehran University of Medical Sciences, Iran;4. Ottawa Hospital Research Institute, Neuroscience, University of Ottawa, Canada;1. Department of Pharmacology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China;2. Research Center for Deepsea Bioresources, Sanya, Hainan 572025, China;3. University of the Chinese Academy of Sciences, Beijing 100049, China;4. The Chinese Academy of Sciences (CAS) Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China;5. The National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China;6. School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China |
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| Abstract: | A method for preparing rat and calf heart slices which retain their responsiveness to various hormones is described. It is shown that isoproterenol and glucagon independently and maximally increased myocardial cyclic AMP, up to about 6-fold, that the stimulatory action of these two hormones was not additive, and that propranolol abolished the action of isoproterenol but not that of glucagon. These data suggest that isoproterenol and glucagon interact with functionally distinguishable receptors on myocardial adenyl cyclase.Acetylcholine antagonized the action of isoproterenol, of glucagon, or of both, greatly reducing the elevation of myocardial cyclic AMP. Acetylcholine also lowered the basal level of cyclic AMP slightly. |
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