Increases in NO₂⁻/NO₃⁻ excretion in the urine as an indicator of the release of endothelium-derived relaxing factor during elevation of blood pressure

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 N^G−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 N^G−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.