1. Under hormonally constant conditions, the effects of a sudden increase in blood pressure on the release of endothelium-derived relaxing factor were evaluated by measuring urinary excretion of NO2/NO3 in rats with renal denervation.

2. Elevation of blood pressure from 136 ± 2 to 153 ± 3 mmHg by an aortic clamp below the renal arteries induced a significant increase in urinary excretion of NO2/NO3 from 76.6 ± 4.2 × 102 to 108.1 ± 8.3 × 102 pmol min−1 g−1 kidney weight (P < 0.05).

3. Infusion of NG−monomethyl-L-arginine (1 mg min−1 kg−1) without an aortic clamp raised mean blood pressure to a similar level; however, urinary excretion of NO2/ NO3 was decreased significantly.

4. During infusion of NG−monomethyl-L-arginine, aortic occlusion caused a significant increase in blood pressure without any changes in NO2/NO3 excretion in the urine.

5. These results suggest that the formation of NO, an indicator of endothelium-derived relaxing factor release, was increased by mechanical pressure elevation without apparent changes in hormonal and neural factors.

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