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Research Article Free access | 10.1172/JCI106442
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 Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37203
Find articles by Kaminsky, N. in: JCI | PubMed | Google Scholar
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 Northcutt, R. in: JCI | PubMed | Google Scholar
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 Hardman, J. in: JCI | PubMed | Google Scholar
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 Sutherland, E. in: JCI | PubMed | Google Scholar
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 Liddle, G. in: JCI | PubMed | Google Scholar
Published December 1, 1970 - More info
Glucagon, infused intravenously into fasting, well-hydrated, normal men in doses of 25-200 ng/kg per min, induced up to 30-fold increases in both plasma and urinary cyclic AMP. Cyclic GMP levels were unaffected by glucagon. Simultaneous cyclic AMP and inulin clearance studies demonstrated that the glucagon-induced increase in urinary cyclic AMP was entirely due to glomerular filtration of the elevated plasma levels of the nucleotide.
The cyclic AMP response to glucagon was not mediated by parathyroid hormone or epinephrine, and trypsintreated glucagon was completely inactive.
The perfused rat liver released cyclic AMP into the perfusate in response to glucagon, indicating that the liver is a possible source of the cyclic AMP entering the extracellular fluids in response to glucagon in vivo.
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