Neurokinin B Is a Paracrine Vasodilator in the Human Fetal Placental Circulation

Neurokinin (NK) B is a member of the tachykinin family of neurotransmitters, exerting hypotensive or hypertensive effects in the mammalian vasculature through synaptic release from peripheral neurons, according to either NK1 and NK2 or NK3 receptor subtype expression, respectively. There is recent e...

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Veröffentlicht in:The journal of clinical endocrinology and metabolism 2003-05, Vol.88 (5), p.2164-2170
Hauptverfasser: Brownbill, P., Bell, N. J., Woods, R. J., Lowry, P. J., Page, N. M., Sibley, C. P.
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container_issue 5
container_start_page 2164
container_title The journal of clinical endocrinology and metabolism
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creator Brownbill, P.
Bell, N. J.
Woods, R. J.
Lowry, P. J.
Page, N. M.
Sibley, C. P.
description Neurokinin (NK) B is a member of the tachykinin family of neurotransmitters, exerting hypotensive or hypertensive effects in the mammalian vasculature through synaptic release from peripheral neurons, according to either NK1 and NK2 or NK3 receptor subtype expression, respectively. There is recent evidence that NKB is expressed by the syncytiotrophoblast of the human placenta, an organ that is not innervated. We hypothesized that NKB is a paracrine modulator of tone in the fetal placental circulation. We tested this hypothesis using the in vitro perfused human placental cotyledon. Our data show that NKB is a dilator of the fetal vasculature, causing a maximal 25.1 ± 4.5% (mean ± sem; n = 5) decrease in fetal-side arterial hydrostatic pressure (5-μm NKB bolus; effective concentration in the circulation, 1.89 nm) after preconstriction with U-46619. RT-PCR demonstrated the presence of mRNA for NK1 and NK2 tachykinin receptors in the placenta. Using selective receptor antagonists, we found that NKB-induced vasodilation is through the NK1 receptor subtype. We found no evidence for the involvement of either nitric oxide or prostacyclin in this response. This study demonstrates a paracrine role for NKB in the regulation of fetal placental vascular tone.
doi_str_mv 10.1210/jc.2002-021727
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Our data show that NKB is a dilator of the fetal vasculature, causing a maximal 25.1 ± 4.5% (mean ± sem; n = 5) decrease in fetal-side arterial hydrostatic pressure (5-μm NKB bolus; effective concentration in the circulation, 1.89 nm) after preconstriction with U-46619. RT-PCR demonstrated the presence of mRNA for NK1 and NK2 tachykinin receptors in the placenta. Using selective receptor antagonists, we found that NKB-induced vasodilation is through the NK1 receptor subtype. We found no evidence for the involvement of either nitric oxide or prostacyclin in this response. 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Lactation ; Receptors, Neurokinin-1 - genetics ; Receptors, Neurokinin-1 - physiology ; Receptors, Neurokinin-2 - genetics ; Receptors, Neurokinin-2 - physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Vasodilation - drug effects ; Vertebrates: reproduction</subject><ispartof>The journal of clinical endocrinology and metabolism, 2003-05, Vol.88 (5), p.2164-2170</ispartof><rights>Copyright © 2003 by The Endocrine Society</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5180-bf731c61759af9dd5f55c5435966949947074483529bf7e22c839fe31d24b47f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=14804006$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12727971$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brownbill, P.</creatorcontrib><creatorcontrib>Bell, N. 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Psychology</subject><subject>Hormone metabolism and regulation</subject><subject>Indomethacin - pharmacology</subject><subject>Neurokinin B - blood</subject><subject>Neurokinin B - pharmacology</subject><subject>Neurokinin B - physiology</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - antagonists &amp; inhibitors</subject><subject>Placenta - blood supply</subject><subject>Placenta - chemistry</subject><subject>Pregnancy. Parturition. 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subjects Biological and medical sciences
Blood Pressure - drug effects
Blood Vessels - drug effects
Blood Vessels - metabolism
Cyclooxygenase Inhibitors - pharmacology
Enzyme Inhibitors - pharmacology
Epoprostenol - physiology
Fetus - blood supply
Fundamental and applied biological sciences. Psychology
Hormone metabolism and regulation
Indomethacin - pharmacology
Neurokinin B - blood
Neurokinin B - pharmacology
Neurokinin B - physiology
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - physiology
Nitric Oxide Synthase - antagonists & inhibitors
Placenta - blood supply
Placenta - chemistry
Pregnancy. Parturition. Lactation
Receptors, Neurokinin-1 - genetics
Receptors, Neurokinin-1 - physiology
Receptors, Neurokinin-2 - genetics
Receptors, Neurokinin-2 - physiology
Reverse Transcriptase Polymerase Chain Reaction
Vasodilation - drug effects
Vertebrates: reproduction
title Neurokinin B Is a Paracrine Vasodilator in the Human Fetal Placental Circulation
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