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Research Article Free access | 10.1172/JCI107609
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
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Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Find articles by Culbert, S. in: JCI | PubMed | Google Scholar
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Find articles by Cook, J. in: JCI | PubMed | Google Scholar
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Find articles by Jennings, A. in: JCI | PubMed | Google Scholar
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Find articles by Burr, I. in: JCI | PubMed | Google Scholar
Published March 1, 1974 - More info
An in vitro system for perifusion of rat pancreatic islets has been utilized to define the effects of cholinergic agents on the dynamics of insulin release. In the absence of glucose the effects of either acetylcholine or acetyl-β-methylcholine were minimal at concentrations up to 10−5 mM. In the presence of low glucose concentration (2.4 mM), both of the muscarinic agents produced dose-dependent biphasic insulin release. Under these conditions significant insulin release was observed over both phases at concentrations of the muscarinic agents as low as 10−8 mM. Further, the dose response curves relating muscarinic concentration to the total amount of insulin released in each of the two phases showed lack of parallelism between the curves. Nicotinic acid in concentrations up to 10−5 mM had no effect on insulin release in the presence of 2.4 mM glucose. When the glucose concentration was increased to 16.4 mM, the effects of the muscarinic agents were significantly less than those observed in the presence of 2.4 mM glucose. This held true whether the effect was defined as absolute increment due to the muscarinic agent or as percentage of enhancement. Atropine inhibited insulin release induced by both acetylcholine and by 16.4 mM glucose. These data indicate that cholinergic stimulation can play a significant role in modifying insulin release patterns.