(Hypertension. 1999;33:487-492.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Renal Nerves Promote Sodium Excretion During Long-Term Increases in Salt Intake
From the Department of Physiology and Biophysics and the Department of Surgery (Cardiothoracic), University of Mississippi Medical Center, Jackson.
Correspondence to Thomas E. Lohmeier, PhD, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505. E-mail tlohmeier{at}physiology.umsmed.edu
Abstract—To determine whether
the renal nerves contribute to sodium homeostasis during long-term
increments in sodium intake, studies were conducted in conscious dogs
subjected to unilateral renal denervation and surgical division of the
urinary bladder into hemibladders to allow separate 24-hour urine
collection from denervated and innervated kidneys. They
were fed a low sodium diet and continuously infused with isotonic
saline (350 mL/d) to provide a daily sodium intake of 
60 mmol.
After control measurements, sodium intake was increased to 470
mmol/d by increasing the rate of isotonic saline infusion to 3000 mL/d
for 5 days; this was followed by a 5-day recovery period.
Twenty-four-hour control values for mean arterial pressure
and ratios for urinary sodium, potassium, and creatinine
excretion from denervated and innervated kidneys (DEN/INN)
were 96±3, 1.06±0.04, 1.00±0.04, and 1.01±0.02 mm Hg,
respectively. During the 8-fold increase in sodium intake, there was
no long-term change in mean arterial pressure, and daily
sodium balance was achieved within 48 hours. Moreover, during the first
day of high salt intake, there were significant reductions in the
DEN/INN for sodium and potassium excretion, which persisted for the
entire 5-day period of increased sodium intake; on day 5, the DEN/INN
for sodium and potassium excretion was 0.86±0.03 and 0.86±0.04,
respectively. In contrast, the DEN/INN for creatinine
excretion remained at control levels during high salt intake.
Furthermore, similar long-term reductions in the DEN/INN for sodium and
potassium excretion occurred in a second group of dogs administered
adrenergic receptor–blocking agents for 5 days to interrupt the
functional effects of the renal nerves. These data indicate that
sustained renal sympathoinhibition promotes sodium and potassium
excretion during long-term increments in sodium intake by inhibiting
tubular reabsorption of these electrolytes.
Key Words: renal nerves • sodium excretion • sodium intake • sympathetic nervous system
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