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Cited by 20Circadian rhythm and melatoninCardiovascular, Neuropeptides, and Oxidative Stress ResearchNitric Oxide and Endothelin Effects

Melatonin potentiates NE-induced vasoconstriction without augmenting cytosolic calcium concentration

Vandeputte, C., Giummelly, P., Atkinson, J., Delagrange, P., Scalbert, E., Capdeville-Atkinson, C.·2001·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.2001.280.1.h420
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Abstract

Because little is known of the intracellular mechanisms involved in the vasoconstrictor effect of melatonin (Mel), we examined the in vitro effects of Mel by using perfused cylindrical segments of the rat tail artery loaded with the intracellular Ca 2+concentration ([Ca 2+]i)-sensitive fluorescent dye, fura 2. Mel (10−14 to 10−4 M) had no effect on baseline perfusion pressure or [Ca 2+]i but increased, at submicromolar concentrations, the vasoconstrictor effect of norepinephrine (NE) ( P = 0.0029). Mel did not modify NE-induced [Ca 2+]i mobilization, and thus the [Ca 2+]i sensitivity of NE-induced contraction increased in the presence of Mel. Mel consistently increased KCl-induced vasoconstriction and [Ca 2+]i sensitivity of contraction, but differences were not statistically significant. In conclusion, Mel increases the [Ca 2+]i sensitivity of vasoconstriction evoked by NE suggesting that Mel may amplify endogenous vasoconstrictor responses to sympathetic outflow.

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Crossref · 10.1152/ajpheart.2001.280.1.h420

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  • The lack of a reduction in arterial blood pressure and forearm vascular resistance during LBNP could be the result of melatonin-induced augmentation of noradrenaline-induced vasoconstriction.

    “The lack of a reduction in arterial blood pressure and forearm vascular resistance during LBNP could be the result of the melatonin-induced augmentation of noradrenaline-induced vasoconstriction (Vandeputte et al. 2001).”

    From Melatonin attenuates the sympathetic nerve responses to orthostatic stress in humans (2003) · cites this paper as Vandeputte et al. 2001

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Authors
Vandeputte, C., Giummelly, P., Atkinson, J., Delagrange, P., Scalbert, E., & Capdeville-Atkinson, C.
Affiliations
  • Université Henri Poincaré (FR)
  • Servier (France) (FR)
  • Laboratoire de Pharmacologie Cardiovasculaire, EA 3116, Faculté de Pharmacie, UHP-Nancy 1, 54001 Nancy Cedex;
ORCID
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2001-01-01
Volume
280
Issue
1
Pages
H420-H425
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.2001.280.1.h420
OpenAlex
W2310485821
Cited by
20
References
31
Citations by year
2026: 2 · 2024: 1 · 2022: 1 · 2021: 1 · 2019: 2 · 2014: 1 · 2012: 1
FWCI
0.47
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
melatonin, norepinephrine, vasoconstriction, intracellular calcium, calcium sensitivity, tail artery, sympathetic vasoconstriction, potassium chloride-induced contraction, calcium mobilization
MeSH terms
Animals, Antioxidants, Arteries, Blood Pressure, Calcium, Cytosol, Drug Synergism, Male, Melatonin, Norepinephrine, Perfusion, Potassium Chloride, Regional Blood Flow, Tail, Vasoconstrictor Agents, Signal Transduction, Rats, Wistar, Rats, In Vitro Techniques

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