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Cardiovascular Research Advance Access [Accepted Manuscript] published online on December 17, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn350
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Role of CuZn Superoxide Dismutase on Carotid Body Function in Heart Failure Rabbits

Yanfeng Ding1, Yu-Long Li2, Matthew C. Zimmerman1, Robin L. Davisson3 and Harold D. Schultz1

1 Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850
2 Department of Emergency Medicine, University of Nebraska Medical Center, Omaha, NE 68198-5850
3 Department of Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY 14853-6401 and Cell and Developmental Biology, Weill Cornell Medical College, New York, NY 10065

1 Correspondence: Harold D. Schultz (Professor) Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850. Tel: (402) 559-7167 Fax: (402)559-4438 E-mail: hschultz{at}unmc.edu

Aims: Peripheral chemoreflex sensitivity is potentiated in both clinical and experimental chronic heart failure (CHF). NADPH oxidase-derived superoxide mediates angiotensin II-enhanced carotid body (CB) chemoreceptor sensitivity in CHF rabbits, and tempol, the superoxide dismutase (SOD) mimetic, inhibits this Ang II- and CHF-enhanced superoxide anion effect. Here we investigated the role of cytoplasmic superoxide dismutase (CuZnSOD) in the CB on chemoreceptor activity and function in CHF rabbits.

Methods and results: CuZnSOD protein expression was decreased in CBs from CHF rabbits vs. sham (p < 0.05). Adenoviral CuZnSOD (Ad CuZnSOD) gene transfer to the CBs increased CuZnSOD protein expression and significantly reduced the baseline renal sympathetic nerve activity (RSNA) and the response of RSNA to hypoxia in the CHF rabbits (p< 0.05). Single-fiber discharge from CB chemoafferents during normoxia (baseline, at ~100 mmHg PO2) and in response to hypoxia were enhanced in CHF vs. sham rabbits (p< 0.05). Ad CuZnSOD decreased the baseline discharge (7.6 ± 1.3 vs. 12.6 ± 1.7 imp/s at ~100 mmHg PO2) and the response to hypoxia (22.4 ± 1.6 vs. 32.3 ± 1.2 imp/s at ~ 40 mmHg PO2, p < 0.05) in CHF rabbits. Ad CuZnSOD also normalized the blunted outward K+ current (IK) in CB glomus cells from CHF rabbits (369 ± 14 vs. 565 ± 31 pA/pF at +70 mV, p < 0.05). In addition, Ad CuZnSOD reduced the elevation of superoxide level in CBs from CHF rabbits.

Conclusion: Downregulation of CuZnSOD in the CB contributes to the enhanced activity of CB chemoreceptors and chemoreflex function in CHF rabbits.

KEYWORDS superoxide dismutase; adenoviral vector; carotid body; sympathetic nerve activity; chemoreceptor; glomus cell; chronic heart failure

Time for primary review: 38 Days


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