Neural control of renal tubular sodium reabsorption of the dog.
The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies demonstrate 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 is prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney upon renal nerve stimulation (angiotensin II, prostaglandin) was excluded by experiments with appropriate blocking agents. Reflex diminutions in renal nerve activity (left atrial distention, stellate ganglion stimulation) produce a decrease in renal tubular sodium reabsorption independent of glomerular filtration rate or renal blood flow. The anatomically described adrenergic innervation of the renal tubules participates in the direct regulation of renal tubular sodium reabsorption.
D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D005919:Glomerular Filtration Rate; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply / Q000294:innervation*; D007684:Kidney Tubules / Q000378:metabolism*; D009318:Natriuresis / Q000187:drug effects; D012039:Regional Blood Flow; D012504:Saralasin / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000502:physiology*
D012964:Sodium; D012504:Saralasin; D007213:Indomethacin