| Leptin impairs cardiovagal baroreflex function at the level of the solitary tract nucleus. | |
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MedLine Citation:
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PMID: 19770402 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Circulating leptin is elevated in some forms of obesity-related hypertension, associated with impaired baroreflex function. Leptin receptors are present on vagal afferent fibers and neurons within the solitary tract nucleus, providing an anatomic distribution consistent with baroreflex modulation. Although solitary tract nucleus microinjection of 144 fmol/60 nL of leptin had no significant effect on baroreflex sensitivity for control of the heart rate in urethane/chloralose-anesthetized Sprague-Dawley rats, 500 fmol of leptin impaired baroreflex sensitivity for bradycardia in response to increases in pressure (1.15+/-0.04 versus 0.52+/-0.12 ms/mm Hg; P<0.01). Transgenic ASrAOGEN rats with low brain angiotensinogen have an upregulation of the leptin receptor and p85 alpha mRNA in the dorsal medulla relative to Sprague-Dawley rats. Consistent with these observations, the response to leptin was enhanced in ASrAOGEN rats, because both the 144-fmol (1.46+/-0.08 versus 0.75+/-0.10 ms/mm Hg; P<0.001) and 500-fmol (1.36+/-0.32 versus 0.44+/-0.06 ms/mm Hg; P<0.05) leptin microinjections impaired baroreflex sensitivity. At these doses, leptin microinjection had no effect on resting pressure, heart rate, or the tachycardic response to decreases in pressure in Sprague-Dawley or ASrAOGEN rats. Thus, exogenous leptin at sites within the solitary tract nucleus impairs the baroreflex sensitivity for bradycardia induced by increases in arterial pressure, consistent with a permissive role in mediating increases in arterial pressure. Baroreflex inhibition was enhanced in animals with evidence of increased leptin receptor and relevant signaling pathway mRNA. |
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Authors:
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Amy C Arnold; Hossam A Shaltout; Patricia E Gallagher; Debra I Diz |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-09-21 |
Journal Detail:
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Title: Hypertension Volume: 54 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2009 Nov |
Date Detail:
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Created Date: 2009-10-22 Completed Date: 2009-11-12 Revised Date: 2010-12-17 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 1001-8 Citation Subset: IM |
Affiliation:
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Hypertension and Vascular Research Center and Physiology and Pharmacology Department, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1032, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Animals Baroreflex / drug effects*, physiology* Bradycardia / metabolism, physiopathology Disease Models, Animal Heart Rate / drug effects*, physiology Leptin / adverse effects, metabolism*, pharmacology* Male Microinjections Probability RNA, Messenger / analysis Random Allocation Rats Rats, Sprague-Dawley Rats, Transgenic Reference Values Sensitivity and Specificity Solitary Nucleus / drug effects*, physiology Sympathetic Nervous System / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-51952/HL/NHLBI NIH HHS; P01 HL051952-150002/HL/NHLBI NIH HHS; P01 HL051952-168199/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Leptin; 0/RNA, Messenger |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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