NITRIC-OXIDE REGULATES RENAL HEMODYNAMICS AND URINARY SODIUM-EXCRETION IN DOGS

The goal of this study was to determine whether nitric oxide has a long-term role in the control of renal hemodynamics and the relation between arterial pressure and urinary sodium excretion. Studies were conducted over a 25-day period in seven conscious dogs equipped with indwelling vascular catheters and an electromagnetic flow probe on the iliac artery. Nitric oxide synthesis was inhibited by continuous intravenous infusion of N-G-nitro-L-arginine methyl ester at 37.1 nmol/kg per minute, and the effects of low, normal, and high sodium intakes were determined. Significant nitric oxide synthesis inhibition was evidenced by a decrease in the depressor and flow responses to systemic acetylcholine administration. During the normal sodium intake plus nitro-arginine period, arterial pressure increased to hypertensive levels, averaging 120 +/- 4% of control; renal vascular resistance increased to an average of 134 +/- 8% of control; glomerular filtration rate and renal plasma flow decreased to 83 +/- 3% and 81 +/- 3% of control, respectively; and no changes occurred in filtration fraction, plasma renin activity, plasma concentrations of aldosterone and cortisol, urinary sodium excretion, sodium balance, fractional excretion of sodium, urine volume, and volume balance. Arterial pressure increased further to 130 +/- 3% of control during high salt intake, and sodium balance was achieved at each sodium intake despite the increase in arterial pressure because of a hypertensive shift in the relation between urinary sodium excretion and arterial pressure. In conclusion, the data suggest that nitric oxide has a long-term role in the regulation of arterial pressure, urinary sodium excretion, and renal vascular resistance during normal, low, and high sodium intakes.