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Department of Pharmacology and Toxicology and Neuroscience Program, Michigan State University, East Lansing, Michigan 48824
The role of
the sympathetic nervous system in 4-hydroxy-2,2,6,6-tetramethyl
piperidinoxyl (tempol)-induced cardiovascular responses in
urethane-anesthetized, normotensive rats was evaluated. Tempol caused
dose-dependent (30-300 µmol/kg iv) decreases in renal
sympathetic nerve activity (RSNA), mean arterial blood pressure (MAP),
and heart rate (HR). Similar responses were obtained after sinoaortic
denervation and cervical vagotomy. These responses were not blocked
following treatment with the nitric oxide synthase inhibitor
NG-nitro-L-arginine (2.6 mg · kg
1 · min1 iv for 5 min) or the 
2-adrenergic receptor antagonist idazoxan (0.3 mg/kg iv bolus). Idazoxan blocked the effects of clonidine (10 µg/kg iv) on HR, MAP, and RSNA. Hexamethonium (30 mg/kg iv) inhibited
RSNA, and tempol did not decrease RSNA after hexamethonium. The effects
of tempol on HR and MAP were reduced by hexamethonium. In conclusion,
depressor responses caused by tempol are mediated, partly, by
sympathoinhibition in urethane-anesthetized, normotensive rats. Nitric
oxide does not contribute to this response, and the sympathoinhibitory
effect of tempol is not mediated via 2-adrenergic receptors. Finally, tempol directly decreases HR, which may contribute to the MAP decrease.
sympathetic nervous system; NG-nitro-L-arginine
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