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Experiments were performed to determine the effects of nitric oxide (NO) synthase inhibition on the renal responses to volume expansion in conscious cynomolgus monkeys. All animals were volume expanded with 3% dextran in normal saline under three conditions: J) during a control state, 2) during constant infusion of the NO synthase inhibitor AF-nitro-L-arginine methyl ester (L-NAME, 30 pg-kg-min"1), and 3) during simultaneous infusion of L-NAME and excess NO substrate L-arginine (0.6 mg-kg1-min1). The control volume expansion increased urine flow from 0.27 0.05 to 0.94 0.28 ml/min and sodium excretion from 21 9 to 95 26 peq/min. During L-NAME infusion, these responses were attenuated in that urine flow only increased from 0.13 0.03 to 0.28 0.09 ml/min and sodium excretion from 13 8 to 35 23 peq/min. Addition of L-arginine to the L-NAME infusion abolished these renal excretory effects of L-NAME alone. With combined L-NAME/L-arginine, volume expansion increased urine flow from 0.37 0.23 to 1.09 0.23 ml/min and sodium excretion from 38 27 to 150 24 peq/min, responses similar to control. L-Arginine also markedly attenuated the effect of L-NAME to increase mean arterial pressure and abolished the L-NAME decreases in creatinine and p-aminohippurate clearances. However, an L-NAME-induced bradycardia could only be partially reversed. These results demonstrate that a functioning NO system may be important in mediating normal renal responses to volume expansion in this primate species. diuresis; natriuresis; nonhuman primate; endotheliumderived relaxing factor Copyright 1997 the American Physiological Society.
American Journal of Physiology - Heart and Circulatory Physiology
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