Functional changes in baroreceptor afferent, central and efferent components of the baroreflex circuitry in Type 1 diabetic mice (OVE26)

    Authors

    H. Gu; P. N. Epstein; L. Li; R. D. Wurster;Z. J. Cheng

    Comments

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    Abbreviated Journal Title

    Neuroscience

    Keywords

    baroreflex; brainstem; baroreceptor; parasympathetic; diabetic; neuropathy; OVE26; AORTIC DEPRESSOR NERVE; HEART-RATE; ELECTRICAL-STIMULATION; TRANSGENIC; MICE; SUDDEN-DEATH; BED SYNDROME; RATS; SENSITIVITY; DYSFUNCTION; MELLITUS; Neurosciences

    Abstract

    Baroreflex control of heart rate (HR) is impaired in diabetes mellitus. We hypothesized that diabetes mellitus induced functional changes of neural components at multiple sites within the baroreflex arc. Type 1 diabetic mice (OVE26) and FVB control mice were anesthetized. Baroreflex-mediated HR responses to sodium nitroprusside- (SNP) and phenylephrine- (PE) induced mean arterial blood pressure (MAP) changes were measured. Baroreceptor function was characterized by measuring the percent (%) change of baseline integrated aortic depressor nerve activity (Int ADNA) in response to SNP- and PE-induced MAP changes. The HR responses to electrical stimulation of the left aortic depressor nerve (ADN) and the right vagus nerve were assessed. Compared with FVB control mice, we found in OVE26 mice that (1) baroreflex-mediated bradycardia and tachycardia were significantly reduced. (2) The baroreceptor afferent function in response to MAP increase did not differ, as assessed by the parameters of the logistic function curve. But, the inhibition of Int ADNA in response to MAP decrease was significantly attenuated. (3) The maximum amplitude of bradycardic responses to right vagal efferent stimulation was augmented. (4) In contrast, the maximum amplitude of bradycardic responses to left ADN stimulation was decreased. Since Int ADNA was preserved in response to MAP increase and HR responses to vagal efferent stimulation were augmented, we conclude that a deficit of the central mediation of baroreflex HR contributes to the overall attenuation of baroreflex sensitivity in OVE26 mice. The successful conduction of physiological experiments on the ADN in OVE26 mice may provide a foundation for the understanding of cellular and molecular mechanisms of diabetes-induced cardiac neuropathy. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.

    Journal Title

    Neuroscience

    Volume

    152

    Issue/Number

    3

    Publication Date

    1-1-2008

    Document Type

    Article

    Language

    English

    First Page

    741

    Last Page

    752

    WOS Identifier

    WOS:000254819900016

    ISSN

    0306-4522

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