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Am J Physiol Heart Circ Physiol 283: H885-H892, 2002. First published May 16, 2002; doi:10.1152/ajpheart.00134.2002
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Vol. 283, Issue 3, H885-H892, September 2002

Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in DOCA-salt rats

Hui Xu, Gregory D. Fink, and James J. Galligan

Department of Pharmacology and Toxicology and The Neuroscience Program, Michigan State University, East Lansing, Michigan 48824

The role of sympathetic nerves and nitric oxide (NO) in tempol-induced cardiovascular responses was evaluated in urethane-anesthetized sham and deoxycorticosterone acetate (DOCA)-salt-treated (DOCA-salt) rats. Tempol (30-300 µmol/kg iv), a superoxide (O<UP><SUB>2</SUB><SUP>−</SUP></UP>) scavenger, decreased renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) in DOCA-salt and sham rats. The antioxidants tiron and ascorbate did not alter MAP, HR, or RSNA in any rat. Tempol responses were unaffected after sham rats were treated with NG-nitro-L-arginine (L-NNA, 13 mg/kg). In DOCA-salt rats, L-NNA reduced tempol-induced depressor responses but not the inhibition of HR or RSNA. Tempol did not significantly decrease MAP, HR, or RSNA after hexamethonium (30 mg/kg iv) treatment in any rat. Dihydroethidine histochemistry revealed increased O<UP><SUB>2</SUB><SUP>−</SUP></UP> levels in arteries and veins from DOCA-salt rats. Tempol treatment in vitro reduced O<UP><SUB>2</SUB><SUP>−</SUP></UP> levels in arteries and veins from DOCA-salt rats. In conclusion, tempol-induced depressor responses are mediated largely by NO-independent sympathoinhibition in sham and DOCA-salt rats. There is an additional interaction between NO and tempol that contributes to depressor responses in DOCA-salt rats.

sympathetic nervous system; deoxycorticosterone acetate


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