Effect on renin release of inhibiting renal nitric oxide synthesis in anaesthetized dogs

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Abstract
Nitric oxide plays an important role in the regulation of basal renal blood flow. This study was performed to examine whether selective inhibiti± of renal nitric oxide synthesis affects renin releasein vivo. Accordingly, in six barbiturate‐anaesthetized dogs renin release was examined before and after intrarenal infusion of the selective inhibitor of nitric oxide synthesis, NG‐nitro‐l‐arginine (NOARG). NOARG was infused into the renal artery to yield a renal arterial blood concentration of 0.4μmol ml‐1. NOARG did not change systemic arterial blood pressure and glomerular filtration rate, but reduced basal renal blood flow by 26 ± 2%. Urine flow, sodium and potassium excretion were reduced after inhibition of renal nitric oxide synthesis. Basal renin release (3 ± 2μg AI min‐1) was not altered by NOARG infusion (1 ± 1μg AI min‐1). To stimulate renin release the renal artery was constricted to a renal perfusion pressure of 50 mmHg. At this perfusion pressure infusion of NOARG reduced renin release significantly from 48 ± 11μg AI min‐1to 14 ± 4μg AI min‐1. In conclusion, inhibition of renal nitric oxide synthesis reduces basal renal blood flow and reduces renin release stimulated by renal arterial constriction. These findings indicate that renal nitric oxide modulates both renal blood flow and renin releasein vivo.