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Suppression of insulin-induced sympathetic activation and vasodilation by dexamethasone in humans.
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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“In lean subjects, sympathetic activation evoked by acute elevation of plasma insulin to high physiological concentrations does not raise blood pressure (12–14)”
From Impaired insulin-induced sympathetic neural activation and vasodilation in skeletal muscle in obese humans. (1994) · cites this paper as [13]
In the citing paper
“In lean healthy subjects, insulin-induced stimulation of muscle blood flow consistently is accompanied by a marked stimulation of sympathetic neural outflow to the same vascular bed (12-14).”
From Impaired insulin-induced sympathetic neural activation and vasodilation in skeletal muscle in obese humans. (1994) · cites this paper as [13]
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Metadata
- Authors
- Scherrer, U., Vollenweider, P., Randin, D., Jéquier, E., Nicod, P., & Tappy, L.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- Venue
- Circulation
- Published
- 1993-08
- Volume
- 88
- Issue
- 2
- Pages
- 388-394
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- 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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