Studies in anesthetized animals suggest that the renal nerves have a role in the regulation of sodium excretion. Urinary sodium excretion decreases when the renal nerves are stimulated and increases after renal denervation or ganglionic blockade. In order to define the role of the renal nerves in the regulation of urinary sodium excretion in awake animals, dogs were prepared with one kidney denervated and the other intact and the bladder split so that urine could be collected from each kidney. Denervation was confirmed by kidney noradrenaline analysis (1.72 ± 0.29 vs 0.18 ± 0.12 nmol/g). These dogs were studied awake with one of two protocols on each of two separate days. In protocol VH, volume expansion (5% body weight) was followed by hemorrhage of 2% body weight. Fractional sodium excretion fell from 4.7 ± 0.5 to 1.1 ± 0.2% on the denervated side and from 5.6 ± 0.6 to 1.4 ± 0.3% on the intact side. Inulin and p-aminohippurate clearance fell similarly on both sides. In protocol HV, hemorrhage of 2% body weight was followed by blood replacement and volume expansion of 5% body weight. In this second protocol fractional sodium excretion during hemorrhage was 0.23 ± 0.07 and 0.24 ± 0.09% for denervated and intact kidneys respectively and increased to 2.04 ± 0.32 and 2.78 ± 0.60 after volume expansion. In both protocols the denervated kidney was able to reabsorb sodium as well as the innervated kidney during hemorrhage and was able to increase fractional sodium excretion as well as the denervated kidney during volume expansion. These results suggest that the renal nerves do not have a significant role in the regulation of sodium excretion in conscious animals.
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