Acute or chronic denervation of the kidney results in a moderate increase in electrolyte and water excretion, often described as a "denerva- tion diuresis" (1-12). The mechanism of the natriuresis that is a feature of this phenomenon remains controversial. A number of investigators (1-5) have suggested that nerves alter sodium excretion indirectly by controlling renal hemodynamics, because in their studies there was a rise in filtered sodium large enough to explain the sodium diuresis. Other workers (6-12) have concluded that denervation depresses tubular transport of sodium. At least two factors probably account for the conflicting conclusions. First, there is the technical problem of accurately measuring the small changes in filtered sodium that occur after section of renal nerves. Second, there are no in- dependent data from which one can determine the effect of an increase in filtered sodium uncomplicated by a change in tubular reabsorptive capacity. Therefore, even if a small increase in filtered so- dium after nerve section is reliably demonstrated, it is uncertain how large an increase in sodium ex- cretion can be ascribed solely to this change. Re- sults that demonstrate a simultaneous rise in so- dium excretion and filtered sodium after denerva- tion, although suggestive, do not conclusively sepa- rate a cause and effect relation from simple association.
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Kamm et al. (1965) studied this question.