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1 Department of Physiology and Biophysics and Medicine, University of Mississippi Medical Center, Jackson, MS, USA
2 Department of Physiopathology, University of Medicine, Asuncion, Paraguay
* To whom correspondence should be addressed. E-mail: jreckelhoff{at}physiology.umsmed.edu.
The roles that NO and plasma renin activity (PRA) play in the depresor response to chronic administration of tempol in SHR are not clear. The present study was done to determine the effect of 2 weeks tempol on blood pressure (MAP), oxidative stress and PRA in the presence or absence of chronic NO synthase inhibition. SHR were divided into four groups: controls, treated with tempol (1 mmol/l) alone, treated with nitro-L-arginine methyl ester (L-NAME; 4.5 mg/kg/d) alone, or treated with tempol plus L-NAME for 2 wks. With tempol, MAP decreased by 22% (control: 191±3; tempol: 162±21 mm Hg; p< 0.05). L-NAME caused a 16% increase in MAP (222±2 mm Hg; p<0.01) and L-NAME/tempol abolished the depressor response to tempol (215±3 mm Hg; p<0.01). PRA was not affected by tempol, but was increased slightly with L-NAME alone and by 4.4 fold with L-NAME/tempol. Urinary nitrate/nitrite increased with tempol and decreased with L-NAME or L-NAME/tempol. Tempol significantly reduced oxidative stress in both the presence or absence of L-NAME. In conclusion, in SHR tempol administration for 2 weeks reduces oxidative stress in the presence or absence of NO, but in the absence of NO, tempol is unable to reduce MAP. Therefore, NO, but not changes in PRA, plays a major role in the BP lowering effects of tempol administration. These data suggest that in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress, but not be able to reduce their blood pressure.
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