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Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge.

Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Research Abstract Details 

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  • Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Abstract Text:

    gwendolen e haleyGwendolen E Haley,francis w flynnFrancis W Flynn,

    Activation of the neurokinin 3 receptor (NK3R) by a receptor agonist, hypotension, and hyperosmolarity results in the internalization of NK3R expressed by magnocellular neurons and the release of vasopressin (VP) and oxytocin (OT) into the circulation. The contribution of NK3R activation to the release of VP and OT in response to hyperosmolarity and hypotension was evaluated by measuring the release of both hormones following pretreatment with a selective NK3R antagonist, SB-222200. Freely behaving male rats were given an intraventricular injection of either 0.15 M NaCl or 250, 500, or 1,000 pmol SB-222200, and then were administered an intravenous infusion of 2 M NaCl or 0.15 M NaCl (experiment 1), or a bolus intra injection of 0.15 M NaCl or hydralazine (HDZ), a hypotension-inducing drug (experiment 2). Blood samples were taken from indwelling arterial catheters at various time points for 1-2 h, both before and after treatments. Plasma VP and OT levels were determined by ELISA. Blockade of NK3R did not affect the baseline levels of either hormone. In contrast, pretreatment with SB-222200 significantly reduced ( approximately 60%) or abolished the release of VP and OT, respectively, to 2 M NaCl infusion. HDZ-induced VP and OT release was eliminated by pretreatment with 500 pmol SB-222200. Therefore, NK3R activation contributes significantly to the systemic release of both VP and OT in response to osmotic and hypotensive challenges.

    Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Publishing Authors By Initials

    ge haleyGE Haley,fw flynnFW Flynn,

    For similar biochemical phenomena, metabolism, and nutrition: biochemical phenomena: water-electrolyte balance research abstracts see: biochemical phenomena, metabolism, and nutrition: biochemical phenomena: water-electrolyte balance research

    PUBMED ID PMID:

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    Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Journal Published:

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

    Journal: American journal of physiology. Regulatory, integr

    VOLUME: 293

    Page Numbers: R931-7

    Journal Abbreviation: Am. J. Physiol. Regul. Integr.

    ISSN: 0363-6119

    DAY: 23

    MONTH: 05

    YEAR: 2007

    Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901230

    Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Keywords Mesh Terms:

    KEYWORDS: Water-Electrolyte Balance

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge. Information

    Substance Name: Hydralazine

    Registry Number: 86-54-4

    Grant and Affiliation Information for Tachykinin NK3 receptor contribution to systemic release of vasopressin and oxytocin in response to osmotic and hypotensive challenge.

    AFFILIATION: Graduate Neuroscience Program, University of Wyoming, Laramie, WY 82071, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCRR

    GRANT: P-20-RR15640

    ACRONYM: RR

    MEDLINETA: Am J Physiol Regul Integr Comp

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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