TY - JOUR
T1 - Effect of intravenous glucagon on urinary catecholamine excretion in normal man
AU - Young, James B.
AU - Landsberg, Lewis
AU - Knopp, Robert H.
N1 - Funding Information:
From the Thorndike Memorial Laboratory, Boston City Hospital and Beth Israel Hospital, rhe Department of Medicine. Harvard Medical School, Boston, Mass., and Harborview Medical Center,-Departmem of Medicine. University of Washington Medical School, Seattle. Wash. Received for publication June I I, 1975. Supported by USPHS Training Grant AM-05060. and Grants HD-08968-01 and FR-76 from the Division of Research Facilities and Resources. Reprint requests should be addressed to Dr. Robert H. Knapp, Northwest Lipid Research Clinic, Harborview Medical Center, 326 Ninth Avenue, Seattle. Wash. 98IO4. 0 I976 bv Grune & Stratton, Inc.
PY - 1976/2
Y1 - 1976/2
N2 - We have evaluated intravenous glucagon as a pharmacologic stimulus to adrenal catecholamine secretion in normal human subjects. Urinary epinephrine and norepinephrine were measured at two hourly intervals before and after the intravenous injection of saline, 4 mg glucagon, or 0.1 μ/kg crystalline insulin. Urinary epinephrine was increased 2.3-fold over baseline after both saline and glucagon. By contrast, insulin hypoglycemia produced a 24-fold rise in urinary epinephrine. No rise in urinary norepinephrine was detected in any test. Under the conditions of this study, we conclude that epinephrine excreted after glucagon injection is due to the stress of the test itself. In normal man, glucagon either does not stimulate adrenal catecholamine secretion, or the effect is too small to measure. By contrast, in pheochromocytoma, glucagon may be specific for catecholamine secretion, based on data from the literature. In normal subjects, insulin hypoglycemia remains the only proved method for assessing adrenal catecholamine reserve.
AB - We have evaluated intravenous glucagon as a pharmacologic stimulus to adrenal catecholamine secretion in normal human subjects. Urinary epinephrine and norepinephrine were measured at two hourly intervals before and after the intravenous injection of saline, 4 mg glucagon, or 0.1 μ/kg crystalline insulin. Urinary epinephrine was increased 2.3-fold over baseline after both saline and glucagon. By contrast, insulin hypoglycemia produced a 24-fold rise in urinary epinephrine. No rise in urinary norepinephrine was detected in any test. Under the conditions of this study, we conclude that epinephrine excreted after glucagon injection is due to the stress of the test itself. In normal man, glucagon either does not stimulate adrenal catecholamine secretion, or the effect is too small to measure. By contrast, in pheochromocytoma, glucagon may be specific for catecholamine secretion, based on data from the literature. In normal subjects, insulin hypoglycemia remains the only proved method for assessing adrenal catecholamine reserve.
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U2 - 10.1016/0026-0495(76)90054-8
DO - 10.1016/0026-0495(76)90054-8
M3 - Article
C2 - 1250159
AN - SCOPUS:0017237190
VL - 25
SP - 233
EP - 237
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
SN - 0026-0495
IS - 2
ER -