1. The enzyme nitric oxide synthase is present in the macula densa and may participate in the control of renin secretion by the adjacent juxtaglomerular cells. In the present study, we investigated the effect of inhibiting nitric oxide synthase on the renin secretory response to frusemide, which stimulates renin secretion by blocking Na+-K+-2Cl co-transport in the macula densa.

2. Injection of frusemide in 12 conscious rabbits elicited a transient increase in mean arterial pressure from 84 ± 2 to 92 ± 3 mmHg at 5 min (P < 0.01) and a sustained increase in heart rate from 246 ± 6 to 281 ± 10 beats/min at 45 min (P < 0.01). Plasma renin activity increased from 8.0 ± 1.2 to 14.3 ± 1.8, 12.4 ± 1.6 and 11.6 ± 1.5 pmol 2 h−1 ml−1 at 15, 30 and 45 min respectively (P < 0.01). There were no changes in plasma sodium and potassium concentrations or osmolality.

3. Inhibition of nitric oxide synthase with NG-nitro-l-arginine methyl ester increased mean arterial pressure by 9 mmHg, decreased heart rate and plasma renin activity, and markedly suppressed the renin response to frusemide (from 4.6 ± 0.7 to 7.6 ± 1.7, 4.7 ± 1.0 and 4.6 ± 0.7 pmol 2 h−1 ml−1 at 15, 30 and 45 min respectively). By contrast, infusion of an equipressor dose of phenylephrine did not suppress the renin response to frusemide.

4. Histochemical studies with the NADPH diaphorase technique confirmed the presence of nitric oxide synthase in the macula densa, and suggested that enzyme activity is increased by treatment with frusemide.

5. These results are consistent with a role for the l-arginine—nitric oxide pathway in the modulation of renin secretion by the macula densa.

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