IMPAIRED BAROREFLEX CONTROL OF RENAL SYMPATHETIC NERVE ACTIVITY IN TYPE 1 DIABETIC MICE (OVE26)

    Authors

    H. Gu; Z. H. Zhang; P. N. Epstein; L. Li; S. W. Harden; R. D. Wurster;Z. J. Cheng

    Comments

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    Abbreviated Journal Title

    Neuroscience

    Keywords

    baroreflex; baroreceptor; sympathetic; neuropathy; nephropathy; diabetes; mellitus; CARDIAC REFLEX SENSITIVITY; BARORECEPTOR REFLEX; SUDDEN-DEATH; ORTHOSTATIC HYPOTENSION; AUTONOMIC NEUROPATHY; EFFERENT COMPONENTS; DIETARY MYOINOSITOL; BED SYNDROME; STREPTOZOTOCIN; MELLITUS; Neurosciences

    Abstract

    To investigate the effects of chronic diabetes on baroreflex control of renal sympathetic nerve activity (RSNA), OVE26 diabetic (transgenic mouse line which develops hyperglycemia within the first 3 weeks after birth) and FVB control mice 5-6 months old were studied. Under anesthesia, RSNA in response to sodium nitroprusside (SNP)- and phenylephrine (PE)-induced mean arterial pressure changes (Delta MAP) were measured. Baroreflex-induced inhibition of RSNA during PE infusion was characterized using the sigmoid logistic function curve. Baroreflex-induced excitation of RSNA during SNP infusion was characterized by the RSNA vs. Delta MAP relationship. Mean arterial pressure (MAP) responses to the left aortic depressor nerve (ADN) stimulation were evaluated. Compared to FVB control, we found in OVE26 mice that (1) RSNA in response to MAP increase during PE infusion was dramatically reduced, as characterized by the maximal gain of the RSNA sigmoid logistic function curve (FVB: -20.0 +/- 5.1; OVE26: -7.6 +/- 0.8%/mm Hg, P < 0.05); (2) RSNA in response to MAP decrease during SNP infusion was also attenuated (P<0.05); (3) MAP responses to ADN stimulation were reduced (P<0.05). We concluded that chronic diabetes impairs baroreflex control of RSNA in OVE26 diabetic mice. The use of the transgenic OVE26 diabetic mouse model may underlie a foundation for the further understanding of diabetes-induced autonomic neuropathy. Published by Elsevier Ltd on behalf of IBRO.

    Journal Title

    Neuroscience

    Volume

    161

    Issue/Number

    1

    Publication Date

    1-1-2009

    Document Type

    Article

    Language

    English

    First Page

    78

    Last Page

    85

    WOS Identifier

    WOS:000266225900011

    ISSN

    0306-4522

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