Neurogenic control of renal tubular sodium reabsorption in the dog: a brief review and preliminary report concerning possible humoral mediation.

The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies have demonstrated adrenergic nerve terminals in direct contact with basement membranes of mammalian renal tubular epithelial cells. Low level direct or baroreceptor reflex stimulation of renal sympathetic nerves produces an increase in renal tubular sodium reabsorption without alterations in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. The antinatriuresis was prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Rat kidney micropuncture studies have localized the site of enhanced tubular sodium reabsorption to the proximal tubule. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney upon renal nerve stimulation was explored. Renal blockade to circulating angiotensin II did not alter the antinatriuretic response to low level direct renal nerve stimulation. Indomethacin was used to inhibit prostaglandin synthesis; this resulted in a rise in mean arterial pressure, a fall in renal blood flow, no significant change in glomerular filtration rate, and a variable fall in urinary sodium excretion. Despite inhibition of prostaglandin synthesis, low level direct renal nerve stimulation produced an increase in renal tubular sodium reabsorption in the absence of changes in renal hemodynamics. Thus, the antinatriuresis of low level direct renal nerve stimulation is not mediated by either circulating angiotensin II or prostaglandin.