Impairment of baroreflex control of heart rate in conscious transgenic mice of type 1 diabetes (OVE26)

    Authors

    M. Lin; S. W. Harden; L. H. Li; R. D. Wurster;Z. X. Cheng

    Comments

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    Abbreviated Journal Title

    Auton. Neurosci-Basic Clin.

    Keywords

    Baroreflex; Nucleus ambiguus; Cardiac ganglia; Heart; OVE26 diabetic; mice; CARDIAC REFLEX SENSITIVITY; AUTONOMIC NEUROPATHY; INDUCED HYPERTENSION; DIETARY MYOINOSITOL; BLOOD-PRESSURE; MELLITUS; DYSFUNCTION; NEPHROPATHY; OVEREXPRESSION; STIFFNESS; Neurosciences

    Abstract

    Baroreflex control of heart rate (HR) is impaired in human type 1 diabetes mellitus. The goal of this study is to use a transgenic mouse model of type 1 diabetes (OVE26) to assess the diabetes-induced baroreflex impairment in the conscious state. OVE26 transgenic mice (which develop hyperglycemia within the first three weeks after birth due to the specific damage of beta cells) and normal control mice (FVB) 5-6 months of age were anesthetized, and the left femoral artery and both veins were catheterized. On the second day after surgery, baroreflex-mediated HR responses to arterial blood pressure (ABP) changes that were induced by separate microinfusion of phenylephrine (PE) and sodium nitroprusside (SNP) at different doses (0.03-0.4 mu g/min) were measured in the conscious state. Compared with FVB control, we found that in OVE26 diabetic mice 1) mean ABP (MABP) and HR were decreased (p < 0.05). 2) PE-induced MABP increases were comparable to those in FVB mice (p > 0.05). 3) Baroreflex-mediated bradycardia was attenuated (p < 0.05). 4) SNP-induced MABP decreases was reduced (p < 0.05). 5) Baroreflex-mediated tachycardia was attenuated (p < 0.05). Since baroreflex control of HR in conscious OVE26 mice is impaired in a similar fashion to human diabetes mellitus, we suggest that OVE26 mice may provide a useful model to study the neural mechanisms of diabetes-induced baroreflex impairment. (C) 2009 Elsevier B.V. All rights reserved.

    Journal Title

    Autonomic Neuroscience-Basic & Clinical

    Volume

    152

    Issue/Number

    1-2

    Publication Date

    1-1-2010

    Document Type

    Article

    Language

    English

    First Page

    67

    Last Page

    74

    WOS Identifier

    WOS:000274572000010

    ISSN

    1566-0702

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