Mechanism of natriuresis after closure of chronic arteriovenous shunts.

Animals subjected to certain cardiovascular manipulations, such as arteriovenous fistulas, diminish their urinary sodium excretion. It has been shown that closure of such fistulas results in a prompt increase in the rate of sodium excretion. However, the nature of the renal mechanisms increasing the excretion of sodium when the initial cardiovascular abnormality is corrected has remained unclear. Since the elucidation of such mechanisms might provide information pertinent to other sodium-retaining states, the effect of closure of chronic Teflon-Silastic arteriovenous shunts was studied in desoxycorticosterone acetate (DOCA)-treated dogs by utilizing micropuncture techniques.Nephron filtration rates were measured first during a control period with open arteriovenous shunts and then again after closure of the shunts in 12 dogs. Nephron filtration rate rose 32% while total glomerular filtration rate (GFR) decreased 8%. After closure of the arteriovenous shunt, fractional reabsorption increased 6%, while total kidney filtration fraction increased from 0.31 to 0.35. Renal plasma flow decreased from a mean of 111 ml/min to 90 ml/min. Closure of the arteriovenous shunts increased sodium excretion from a mean of 21 mueq/min to 45 mueq/min. Concomitantly, a redistribution of filtrate to superficial nephrons occurred. Since pharmacological doses of DOCA were being administered while total GFR was not increased and fractional reabsorption of sodium in the proximal tubule was not inhibited, it was concluded that filtrate distribution to superficial nephrons may have contributed to the observed natriuresis, although alternate explanations were also deemed possible.