Renal neuroadrenergic transmission.
To study the role of the renal sympathetic nerves in the regulation of sodium excretion, we examined the renal functional response to left renal nerve stimulation before (group I) and after (group II) left renal adrenergic blockade with guanethidine. In group I dogs, absolute sodium excretion from the left kidney fell markedly after left renal nerve stimulation; the decreases in glomerular filtration rate and renal blood flow were of a similar magnitude. Using the radiolabeled microsphere technique, distribution of renal blood flow to the outer cortex was diminished after left renal nerve stimulation. In group II dogs, guanethidine blocked all of these effects of left renal nerve stimulation. In group iii studies, a low level of left renal nerve stimulation was used which resulted in a decrease in sodium excretion in the absence of changes in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow; this effect was blocked by renal adrenergic blockade with guanethidine in group iv studies. These data support a role for the renal sympathetic nerves to directly influence renal tubular sodium transport in the absence of alterations in renal hemodynamics.
D000818:Animals; D001794:Blood Pressure; D001798:Blood Proteins / Q000032:analysis; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D005919:Glomerular Filtration Rate; D006145:Guanethidine / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply / Q000294:innervation* / Q000502:physiology; D007672:Kidney Cortex / Q000098:blood supply; D012039:Regional Blood Flow; D012964:Sodium / Q000378:metabolism / Q000652:urine*; D013564:Sympathetic Nervous System / Q000502:physiology*
D001798:Blood Proteins; D012964:Sodium; D006145:Guanethidine