Mechanism of Natriuresis after Closure of Chronic Arteriovenous Shunts

Abstract

A B S T R A C T 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 vith open arteriovenous shunts and then again after closure of the shun.s 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 21Aeq/min to 45 Aeq/min. Concomitantlv, a redistribution of filtrate to superficial nephrons occurred. Since pharmacological doses of DOCA wvere being administered while total GFR was not increased and fractional reaisorption 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.

Functional Compensatory Changes after Unilateral Nephrectomy in Rats

“…This, in turn, could lead to activation of baroreceptors, subsequently producing reflex cardiovascu lar changes and increased cation excretion [5] . This effect was similar to that produced by the closure of a chronic arteriovenous fis tula [21]. Our studies have been performed 48 h after U N X , a period in which some other compensatory mechanisms could well be active and responsible for the different hemodynamic changes observed.…”

Role of Hemodynamic Changes in the Increased Cation Excretion after Acute Unilateral Nephrectomy in the Anesthetized Dog

“…Whether the fall in RBF in the present studies was associated with a redistribution of blood flow to lead to natriuresis is not known; earlier reports failed to demonstrate measurable blood flow redistribution after AUN (2,26). On the other hand, redistribution of GFR to superficial cortical nephrons has been observed 15 h after uninephrectomy (27) and immediately' on closure of an A-V fistula (22). How such redistribution occurs, and its consequences on proximal tubular sodium, bicarbonate, and phosphate reabsorption, remain questions for further study.…”

“…If AUN causes only trivial changes in right-sided cardiac pressures, as has been reported to be the case on closure of an A-V fistula (16,17), then antinatriuretic stimuli arising from activation of right atrial receptors would be minimal or absent (19)(20)(21). A further parallel between these two maneuvers is the observation of decreased RPF on closure of an A-V fistula (22). The pattern of anion excretion seen on closing a fistula is not known, but would have to include phosphaturia and bicarbonaturia without chloruresis in order to be consistent with the observations after AUN. The present studies show clearly that the renal nerves or changes in mineralocorticoid activity are not necessary for the response, in accord with earlier observations (2,6,14).…”