Biphasic effect of epinephrine on blood glucose during hyperinsulinemia in borderline hypertensive young men

• Published in: American journal of hypertension Vol. 14; no. 6; pp. 539 - 545
• Main Authors: Høieggen, Aud, Fossum, Eigil, Moan, Andreas, Rostrup, Morten, Eide, Ivar K., Kjeldsen, Sverre E.
• Format: Journal Article
• Language: English
• Published: New York, NY Oxford University Press 01-06-2001; Elsevier Science
• Subjects: Adolescent; Analysis of Variance; Area Under Curve; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood glucose; Blood Glucose - drug effects; Blood Glucose - metabolism; Blood Pressure - drug effects; Cardiology. Vascular system; catecholamines; Catecholamines - administration & dosage; Catecholamines - blood; Catecholamines - pharmacology; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Epinephrine - administration & dosage; Epinephrine - blood; Epinephrine - pharmacology; Glucose - administration & dosage; Heart Rate - drug effects; Humans; Hyperinsulinism - blood; Hypertension - blood; Hypertension - physiopathology; Insulin - administration & dosage; Insulin - blood; insulin sensitivity; Male; Medical sciences; sympathetic nervous system; Sympathetic Nervous System - physiopathology; Epinephrine; Human; Pharmacologic test; Cardiovascular disease; Sympathetic nervous system; Borderline hypertension; Glycemia
• ISSN: 0895-7061; 1941-7225; 1879-1905
• DOI: 10.1016/S0895-7061(00)01306-6

We aimed to study the glycemic response to epinephrine during hyperinsulinemia and infused epinephrine (0.03 μg/kg/min) for 30 min after 90 min of hyperinsulinemic glucose clamp in 14 borderline hypertensive young men. Plasma epinephrine was increased from 0.34 ± 0.08 to 2.33 ± 0.33 nmol/L while insulin and glucose infusions were kept constant with consequent changes in blood glucose. Initially (90 to 95 min), there was a decrease in blood glucose (P = .016) that correlated negatively with glucose disposal rate corrected for insulin (r = −0.55, P = .040) and positively with fasting insulin (r = 0.55). Thereafter, there was an increase in blood glucose (95 to 120 min) (P < .001) that persisted during the recovery period (120 to 140 min). The glucose increase (90 to 140 min) correlated positively with fasting insulin (r = 0.55), systolic blood pressure (r = 0.57), Δ epinephrine 90 to 120 min (r = 0.59), and baseline epinephrine (r = 0.57). Blood glucose remained unchanged (P = .207) in a saline control group (n = 6) with a significant group × treatment effect versus epinephrine (P = .003). Thus, epinephrine caused a biphasic response in blood glucose during hyperinsulinemia. The initial dip in glucose was more pronounced with higher insulin sensitivity, corresponding to previous observations during mental stress test. The following increment in blood glucose was positively related to insulin, systolic blood pressure, and epinephrine levels. These data suggest that insulin may modify the glycemic response to epinephrine in a potentially favorable direction and indicate some lag time before epinephrine gains effect. Subjects who are insulin sensitive and have low blood pressure and resting epinephrine levels seem to be less prone to hyperglycemia induced by epinephrine. Am J Hypertens 2001;14:539–545 © 2001 American Journal of Hypertension, Ltd.