The superoxide dismutase mimetic, tempol, reduces the bioavailability of nitric oxide and does not alter L-NAME-induced hypertension in rats.

L-NAME-induced hypertension is characterized by chronic inhibition of nitric oxide synthesis. We have investigated if tempol, an agent mimicking superoxide dismutase might reduce hypertension and the increased vascular reactivity to pressor agents. Rats were divided into: Control, animals receiving L-NAME 50 mg kg(-1)day(-1), tempol 200 mg kg(-1)day(-1) and tempol plus L-NAME. Drugs were administrated in the drinking water for seven days. L-NAME increased mean arterial blood pressure (Control: 108+/-3 mmHg versus L-NAME 181+/-5 mmHg; P<0.05). Tempol did not change arterial pressure and heart rate in L-NAME and Control groups. The reactivity to phenylephrine increased in the L-NAME group (E(max) Control: 2.00+/-0.15 g versus L-NAME: 2.45+/-0.14 g); tempol+L-NAME (E(max): 2.55+/-0.15 g) and in the tempol group (E(max): 2.57+/-0.14 g). Maximal relaxation induced by acetylcholine was reduced in L-NAME group (60.9+/-3%) and tempol+L-NAME (37.4+/-6%) compared to Control (99.1+/-0.12%) and tempol groups (95.6+/-2.12%). All treated groups presented a reduction in the effects of L-NAME administration on basal vascular tone. Our results show that tempol, in the dose used in this study, did not change the effects of L-NAME on blood pressure which suggests that tempol reduces bioavailability of nitric oxide on aortic isolated ring.