Contribution of nitric oxide, angiotensin II and superoxide dismutase to exercise-induced attenuation of blood pressure elevation in spontaneously hypertensive rats.

Abstract

Moderate chronic exercise attenuates the elevation of blood pressure in young spontaneously hypertensive rats. In order to elucidate the physiological process of the effects of exercise, we examined the involvement of nitric oxide, angiotensin II, and superoxide dismutase in this process. Rats were exercised by voluntary running in a wheel-cage for 10 weeks. Systolic blood pressure in the exercised rats (195+/-4 mmHg, n=27) was significantly (p<0.05) lower than in the post-control rats (212+/-3 mmHg, n=28). The concentration of total plasma nitrite was significantly higher in exercised rats (14.9+/-1.5 micromol l(-1)) than in the post-control rats (9.9+/-0.7 micromol l(-1), p<0.05). Superoxide dismutase activity in the exercised rats was significantly higher (p<0.05) than in the post-control rats (thoracic aorta: 4.6+/-0.3 U mg protein(-1) vs 3.6+/-0.3 U mg protein(-1), heart: 12.7+/-0.6 U mg protein(-1) vs 10.2+/-0.6 U mg protein(-1), p<0.05). The plasma angiotensin II concentration was higher in the post-control rats (74.4+/-14.0 pg mL(-1)) than in the exercised rats (45.0+/-6.4 pg mL(-1), p<0.05), and in the pre-control rats (47.2+/-6.0 pg mL(-1)). The results suggest that exercise acts to decrease the level of superoxide by increasing superoxide dismutase activity in the aorta and heart and to decrease levels of angiotensin II, both of which, in turn, increase the effective concentration of nitric oxide. We conclude that the combination of these effects with the increased NO formation resulted in the low blood pressure seen in the exercised rats.