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Functional Changes in Baroreceptor Afferent, Central, and Efferent Components of the Baroreflex Circuitry in Type 1 Diabetic Mice (OVE26)
Author(s) -
Gu He,
Epstein Paul N,
Li Lihua,
Wurster Robert D,
Cheng Zixi Jack
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.950.7
Subject(s) - baroreflex , baroreceptor , efferent , reflex bradycardia , medicine , bradycardia , heart rate , blood pressure , phenylephrine , mean arterial pressure , stimulation , reflex , endocrinology , vagus nerve , anesthesia , afferent
Baroreflex control of heart rate (HR) is impaired in diabetes mellitus. We hypothesized that diabetes induced functional changes of the neural components at multiple sites within the baroreflex arc. OVE26 diabetic 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 afferent function was characterized by measuring the percent change of the baseline of integrated aortic depressor nerve activity (Int ADNA) in response to MAP changes. The HR responses to electrical stimulation of the left aortic depressor nerve and the right vagus nerve were assessed. Compared to FVB control mice, we found in OVE26 mice that (1) Reflex‐mediated bradycardia and tachycardia were reduced (p<0.05). (2) The baroreceptor afferent function in response to MAP increase did not differ (p>0.05), as assessed by the parameters of the logistic function curve. But, the inhibition of Int ADNA in response to MAP decrease was attenuated (p<0.05). (3) The maximum amplitude of HR responses to right vagal efferent stimulation was augmented (P<0.05). (4) The maximum amplitude of HR responses to left ADN stimulation was decreased (p<0.05). We conclude that a selective deficit of central mediation of reflex bradycardia contributes to the overall attenuation of baroreflex control of HR in OVE26 mice.