Cited by 131Cardiovascular and exercise physiologyDiabetes, Cardiovascular Risks, and LipoproteinsBlood Pressure and Hypertension Studies

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Suppression of insulin-induced sympathetic activation and vasodilation by dexamethasone in humans.

Scherrer, U, Vollenweider, P, Randin, D, Jéquier, E, Nicod, P, Tappy, L·1993·Circulation

DOI 10.1161/01.cir.88.2.388

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Abstract

Background Physiological hyperinsulinemia in lean human subjects stimulates sympathetic nerve activity and blood flow in skeletal muscle, but the underlying mechanism is unknown. Potential mechanisms include central neural or peripheral actions of insulin. Glucocorticoids may potentially interfere with both such actions and thereby may attenuate sympathoexcitatory and vasodilatory effects of insulin in skeletal muscle. Methods and results To determine whether insulin-induced sympathetic activation and vasodilation are attenuated by dexamethasone, we measured muscle sympathetic nerve activity and muscle blood flow during euglycemic hyperinsulinemia before and after short-term administration of this pharmacological agent. Insulin concentrations, which normally doubled sympathetic activity and markedly increased blood flow, had no such stimulatory effect after short-term dexamethasone administration. In contrast, responses to two noninsulin sympathetic stimuli, the Valsalva maneuver and immersion of the hand in ice water, and the vasodilatory response to calf vascular occlusion were not altered by dexamethasone. Conclusions These results demonstrate a dramatic impairment of insulin-induced sympathetic activation and vasodilation by dexamethasone in lean, healthy humans. This study suggests that dexamethasone administration to lean subjects may offer an experimental model to examine underlying mechanisms that regulate the interplay between cardiovascular, sympathetic, and metabol…

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Authors: Scherrer, U., Vollenweider, P., Randin, D., Jéquier, E., Nicod, P., & Tappy, L.
Affiliations: Centre Hospitalier Universitaire Vaudois (CH)
ORCID: Vollenweider, P
Tappy, L
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1993-08
Volume: 88
Issue: 2
Pages: 388-394
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/01.cir.88.2.388
OpenAlex: W2026983353
Cited by: 131
References: 42
Citations by year: 2025: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 1 · 2019: 4 · 2018: 3 · 2016: 1 · 2015: 2 · 2014: 3 · 2013: 2 · 2012: 2
FWCI: 16.23
Type: journal article
Language: en
Open access: closed
Locations: Circulation (publishedVersion)
PubMed (publishedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
Keywords: insulin, dexamethasone, glucocorticoids, sympathetic activity, muscle blood flow, euglycemic hyperinsulinemia, vasodilation, skeletal muscle, Valsalva maneuver, cold pressor response, vascular occlusion, sympathoexcitation
MeSH terms: Adult, Dexamethasone, Electrophysiology, Glucose, Humans, Insulin, Insulin Antagonists, Leg, Muscles, Plethysmography, Regional Blood Flow, Sympathetic Nervous System, Vascular Resistance, Vasodilation, Glucose Clamp Technique

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Suppression of insulin-induced sympathetic activation and vasodilation by dexamethasone in humans.

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