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Impaired Baroreflex Control of Renal Sympathetic Nerve Activity (RSNA) and Elevated Basal RSNA in Type 1 Diabetic Mice (OVE26)
Author(s) -
Gu He,
Zhang Zhihua,
Epstein Paul N.,
Li Lihua,
Harden Scott . W,
Wurster Robert D.,
Cheng Zixi Jack
Publication year - 2009
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.23.1_supplement.610.7
Subject(s) - baroreflex , medicine , phenylephrine , sodium nitroprusside , endocrinology , basal (medicine) , stimulation , anesthesia , diabetes mellitus , blood pressure , heart rate , nitric oxide
To investigate the effects of chronic diabetes on baroreflex control of renal sympathetic nerve activity (RSNA) and basal RSNA, OVE26 diabetic (transgenic mouse line which develops hyperglycemia within the first three 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 (ΔMAP) 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. ΔMAP relationship. MAP responses to the left aortic depressor nerve (ADN) stimulation were evaluated. Basal RSNA was estimated as the resting RSNA divided by the maximal RSNA measured during SNP‐infusion. 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 %/mmHg, 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); (4) the basal RSNA was elevated (P<0.05). We concluded that chronic diabetes impairs baroreflex control of RSNA and elevates basal 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. Supported by NIH HL79636.