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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00134.2002
Submitted on February 21, 2002
Accepted on May 8, 2002
1 Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA
* To whom correspondence should be addressed. E-mail: galliga1{at}msu.edu.
The role of sympathetic nerves and nitric oxide (NO) in tempol-induced cardiovascular responses was evaluated in urethane-anesthetized sham and DOCA-salt rats. Tempol (30-300 µmol/kg, i.v.), a superoxide (O2-) 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 treating sham rats 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, i.v.) treatment in any rat. Dihydroethidine histochemistry revealed increased O2- levels in arteries and veins from DOCA-salt rats. Tempol treatment in vitro reduced O2- levels in arteries and veins from DOCA-salt rats. In conclusion, tempol-induced depressor responses are mediated largely by NO-independent sympatho-inhibition in sham and DOCA-salt rats. There is an additional interaction between NO and tempol that contributes to depressor responses in DOCA-salt rats.
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