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Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons.

Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Research Abstract Details 

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  • Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Abstract Text:

    satoshi fujitaSatoshi Fujita,maryann bohlandMaryann Bohland,graciela sanchez-wattsGraciela Sanchez-Watts,alan g wattsAlan G Watts,casey m donovanCasey M Donovan,

    To elucidate the type of spinal afferent involved in hypoglycemic detection at the portal vein, we considered the potential role of capsaicin-sensitive primary sensory neurons. Specifically, we examined the effect of capsaicin-induced ablation of portal vein afferents on the sympathoadrenal response to hypoglycemia. Under anesthesia, the portal vein was isolated in rats and either capsaicin (CAP) or the vehicle (CON) solution applied topically. During the same surgery, the carotid artery (sampling) and jugular vein (infusion) were cannulated. One week later, all animals underwent a hyperinsulinemic hypoglycemic clamp, with glucose (variable) and insulin (25 mU x kg(-1) x min(-1)) infused via the jugular vein. Systemic hypoglycemia (2.76 +/- 0.05 mM) was induced by minute 75 and sustained until minute 105. By design, no significant differences were observed in arterial glucose or insulin concentrations between groups. When hypoglycemia was induced in CON, the plasma epinephrine concentration increased from 0.67 +/- 0.05 nM at basal to 36.15 +/- 2.32 nM by minute 105. Compared with CON, CAP animals demonstrated an 80% suppression in epinephrine levels by minute 105, 7.11 +/- 0.55 nM (P < 0.001). A similar response to hypoglycemia was observed for norepinephrine, with CAP values suppressed by 48% compared with CON. Immunohistochemical analysis of the portal vein revealed an 85% decrease in the number of calcitonin gene-related peptide-reactive nerve fibers following capsaicin-induced ablation. That the suppression in the sympathoadrenal response was comparable to our previous findings for total denervation of the portal vein indicates that hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons.

    Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Publishing Authors By Initials

    s fujitaS Fujita,m bohlandM Bohland,g sanchez-wattsG Sanchez-Watts,ag wattsAG Watts,cm donovanCM Donovan,

    For similar surgical procedures, operative: neurosurgical procedures: denervation: autonomic denervation: sympathectomy: sympathectomy, chemical research abstracts see: surgical procedures, operative: neurosurgical procedures: denervation: autonomic denervation: sympathectomy: sympathectomy, chemical research

    PUBMED ID PMID:

    MEDLINE DATE:

    Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: American journal of physiology. Endocrinology and

    VOLUME: 293

    Page Numbers: E96-E101

    Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

    ISSN: 0193-1849

    DAY: 20

    MONTH: 03

    YEAR: 2007

    Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901226

    Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Keywords Mesh Terms:

    KEYWORDS: Sympathectomy, Chemical

    MESH TERMS: innervation

    Chemical & Substance for Abstract: Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons. Information

    Substance Name: Capsaicin

    Registry Number: 404-86-4

    Grant and Affiliation Information for Hypoglycemic detection at the portal vein is mediated by capsaicin-sensitive primary sensory neurons.

    AFFILIATION: Department of Kinesiology, University of Southern California, Los Angeles, California 90089, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS-029728

    ACRONYM: NS

    MEDLINETA: Am J Physiol Endocrinol Metab

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    Number Hits: 0

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