Nitric oxide synthase inhibition aggravates the adverse renal effects of high but not low intraabdominal pressure.

Background: Previously, the authors demonstrated that an intraabdominal pressure (IAP) of 14 mmHg in normal rats reduced kidney function/hemodynamics. These adverse effects are related to interference with the nitric oxide (NO) system. This study was designed to compare the effects of NO synthase (NOS) inhibition on kidney function/hemodynamics during increases in IAP from 0 mmHg to 7, 10, and 14 mmHg.

Methods: The rats were divided into six groups. After an IAP of 0 (baseline), the first three groups were subjected to increasing IAPs as follows: 7 mmHg (group 1), 10 mmHg (group 2), and 14 mmHg (group 3). Each pressure was applied for 1 h, followed by a deflation period of 60 min (recovery). An additional three groups were pretreated with nitro-L: -arginine methyl ester (L: -NAME), an NOS inhibitor, before pressures of 7 mmHg (group 4), 10 mmHg (group 5) and 14 mmHg (group 6) were applied for 1 h. Urine flow rate (V), Na(+) excretion (U(Na)V), glomerular filtration rate (GFR), and renal plasma flow (RPF), were determined throughout the experiments.

Results: There were no significant changes in V, U(Na)V, GFR, or RPF during 7-mmHg insufflation. However, significant reductions in these parameters were observed during 10 and 14 mmHg, with V decreasing from 9.95 + or - 1.34 microl/min to 6.8 + or - 1.1 and 6.1 + or - 0.5 microl/min (p < 0.05) and U(Na)V decreasing from 1.29 + or - 0.28 to 0.43 + or - 0.32 muEq/min (p < 0.05), and 0.39 + or - 0.09 muEq/min (p < 0.05). These alterations in excretory functions were associated with considerable declines in GFR, from 1.98 + or - 0.2 to 1.05 + or - 0.18 ml/min (p < 0.05) and 0.95 + or - 0.06 ml/min (p < 0.05) and RPF from 8.66 + or - 0.62 to 3.94 + or - 0.88 ml/min (p < 0.05) and 3.08 + or - 0.71 ml/min (p < 0.05), respectively. When the animals were pretreated with L: -NAME, the adverse renal effects of an IAP of 14 mmHg, but not 10 mmHg, were substantially aggravated.

Conclusion: Decreased renal function/perfusion is induced by IAP pressures of 10 and 14 mmHg but not 7 mmHg. Inhibition of NOS aggravates the adverse renal effects of high (14 mmHg) but not low (7 or 10 mmHg) IAP, indicating that NO deficiency may contribute to the renal dysfunction during high IAP.