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Ergot alkaloid consumption alters serotonin receptor-induced vasoactivity in ovine umbilical vasculature

  • James L. Klotz
  • , Jessica L. Britt
  • , Maslyn A. Greene
  • , Coral Kent-Dennis
  • , Susan K. Duckett

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Consumption of ergot alkaloids during the second half of gestation has been shown to decrease umbilical artery vasoactivity resulting in decreased birth weights. Negative vascular effects of ergot alkaloids are mediated predominantly through serotonergic and adrenergic receptors in other tissues. Vasoactivity of serotonin (5-HT) receptors 5-HT2A and 5-HT1B/1D in umbilical artery and vein from ewes receiving endophyte-infected seed (E + 1.77 mg ergovaline/hd/d) or a control total mixed ration (CON; 0 mg ergovaline/hd/d) tall fescue seed at d-110 and d-133 of gestation was evaluated. Gravid reproduction tracts were collected from ewes. Two-mm sections of umbilical artery and vein were exposed to increasing concentrations of a 5-HT1B/1D agonist and 5-HT2A agonist. The 5-HT1B/1D agonist did not stimulate a contractile response in artery or vein or either gestation time point. 5-HT2A agonist caused large responses in artery with greatest occurring at d-110 and decreasing in magnitude as days of gestation increased (p < 0.05). On d-110 and 133 of gestation, arteries from CON ewes had greater contractile response than arteries collected from E+ ewes (p < 0.05). Veins responded to increasing concentrations of the 5-HT2A agonist. Maximal d-110 vein response was greater than d-133 when exposed to 5-HT2A agonist (p < 0.05). Unlike the artery, veins from E+ ewes had greater d-133 contractile response than CON (p < 0.05). Vascular contractions of umbilical artery and vein are induced by 5-HT2A receptor activity and not 5-HT1B/1D. Umbilical artery 5-HT2A receptor activity was more sensitive to seed treatment and could be responsible for ergot alkaloid-induced intra-uterine growth restriction.

Original languageEnglish
JournalHuman and Experimental Toxicology
Volume43
DOIs
StatePublished - Jan 1 2024

Bibliographical note

Publisher Copyright:
© The Author(s) 2024.

Funding

The authors would like to acknowledge with gratitude the technical support of Adam J. Barnes of the USDA-ARS Forage-Animal Production Research Unit. Mention of trade name, proprietary product of specified equipment does not constitute a guarantee or warranty by the USDA and does not imply approval to the exclusion of other products that may be available. USDA is an equal opportunity provider and employer. The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the USDA-ARS National Program 101 – Food Animal Production, Project Plan Number: 5042-32630-004-000-D, was based upon work supported by NIFA/USDA under project # SC-1700537 of the Clemson University Experiment Station, and was supported in part by an appointment to the Agricultural Research Service (ARS) Research Participation Program administered by the Oak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. All opinions expressed in this paper are the author’s and do not necessarily reflect the policies and views of USDA, DOE, or ORAU/ORISE. The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the USDA-ARS National Program 101 – Food Animal Production, Project Plan Number: 5042-32630-004-000-D, was based upon work supported by NIFA/USDA under project # SC-1700537 of the Clemson University Experiment Station, and was supported in part by an appointment to the Agricultural Research Service (ARS) Research Participation Program administered by the Oak Ridge Institute for Science and Education (ORISE) through an interagency agreement between the U.S. Department of Energy (DOE) and the U.S. Department of Agriculture (USDA). ORISE is managed by ORAU under DOE contract number DE-SC0014664. All opinions expressed in this paper are the author’s and do not necessarily reflect the policies and views of USDA, DOE, or ORAU/ORISE.

FundersFunder number
USDA-ARS Forage-Animal Production Research Unit
Clemson University Experiment Station
Oak Ridge Institute for Science and Education
U.S. Department of Energy
U.S. Department of Agriculture
USDA-Agricultural Research Service5042-32630-004-000-D
US Department of Agriculture National Institute of Food and Agriculture, Agriculture and Food Research InitiativeSC-1700537
Oak Ridge Associated UniversitiesDE-SC0014664

    Keywords

    • Ergot alkaloids
    • Ewe
    • gestation
    • serotonin
    • vasoconstriction

    ASJC Scopus subject areas

    • Toxicology
    • Health, Toxicology and Mutagenesis

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