The mechanism of the reflex depressor function from the kidney was studied in anesthetized dogs with penthobarbitone sodium under artificial breathing.
The action potentials of the efferent renal nerve (sympathetic) decreased by compression of the kidney and renal vein occlusion, and were followed by a fall in the systemic arterial pressure. The efferent action potentials were slightly increased or unchanged by renal artery occlusion but were followed by a rise in the systemic arterial pressure.
The action potentials of the afferent renal nerve increased with the rise in the intrarenal pressure produced by compression of the kidney, by renal vein occlusion, and by elevation of the perfusion pressure of the kidney in cross-perfusion experiments.
The afferent discharge decreased with the fall in the intrarenal pressure produced by renal artery occlusion. The action potentials of the efferent nerve decreased by electric stimulation of the afferent nerve, and were followed by a fall in the systemic arterial pressure. The action potentials of the afferent nerve evoked by compression of the kidney, by elevation of the intrapelvic pressure, and by renal vein occlusion, did not vanish after subcapsular and intrapelvic injection of 2% procaine or after total decapsulation. The evoked action potentials disappeared after injection of procaine into the renal artery.
It was concluded from these data that the receptor, which is sensitive to the changes of the intrarenal pressure, is activated by elevation of the intrarenal pressure and causes reflex hypotension by means of the inhibition of the sympathetic discharge.