Effect of dilution and expansion of blood volume on proximal sodium reabsorption

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.

Section: Resultssupporting

confidence: 41%

Mechanism of Natriuresis after Closure of Chronic Arteriovenous Shunts

Mandin¹

1973

“…That inhibition of proximal reabsorption can occur without sodium diuresis has been demonstrated by micropuncture experiments (17,18). The extent to which Na+,K+-ATPase participates in proximal reabsorption can be further examined during the high-dose experiments.…”

Section: Discussionmentioning

confidence: 98%

Renal Sodium-Potassium-Activated Adenosine Triphosphatase and Sodium Reabsorption

Martinez-Maldonado¹,

Allen²,

Inagaki³

et al. 1972

A B S T R A C T The role of renal Na+,K+-ATPase in sodium reabsorption was further examined in dogs in which digoxin, a specific inhibitor of the enzyme system, was infused into one renal artery in doses ranginig from 0.4 to 0.9 /Ag/kg/min (low dose) and from 1.0 to 4.0 Ag/kg/ min (high dose). A significant natriuresis occurred with both dose ranges which was accompanied by inhibition of Na+,K+-ATPase of cortex and nmedulla in the infused kidney. Despite over 90% enzyme inhibition in many experiments, at least 80% of the filtered sodium continued to be reabsorbed. The per cent change in enzyme activity correlated with the rate of digoxin administration and the total dose administered but not with changes in sodium excretion. Changes in medullary Na+,K+-ATPase activity, however, bore a direct relationship to alterations in fractional solute free water reabsorption (TcH1o). Inhibition of cortical enzyme activity alone was not associated with natriuresis, suggesting that medullary enzyme activity must be depressed for increased sodium excretion to occur during digoxin infusion. In high-dose experiments, significant inhibition of cortical and medullary enzyme in the contralateral control kidney was also observed, but natriuresis did not occur. In these experiments the rate at which digoxin reached the control kidney rose progressively but never equaled the rates in the directly infused kidney with either dose. Nevertheless, it is clear that under certain circumstances enzyme inhibition of either cortex or medulla need not be accompanied by natriuresis. We conclude that the major role of renal Na+,K+-ATPase is in sodium reabsorption in the medulla (ascending limb of Henle's loop) and that it has a relatively small role in proximal sodium reabsorption. The Dr. Tsaparas is a Hoechst International Fellow in Nephrology.

“…The rise in hematocrit that accompanied volume depletion might also have affected proximal tubular function by changing the viscosity of the blood and the flow and pressure in peritubular capillaries (23,24). Neither hydrostatic pressure in peritubular capillaries nor systemic blood pressure was measured in these experiments; it is conceivable that these "physical factors" might have influenced reabsorption from the proximal tubule (25).…”

Section: Discussionmentioning

confidence: 99%

Accelerated reabsorption in the proximal tubule produced by volume depletion

Weiner¹,

Weinman²,

Kashgarian³

et al. 1971

A B S T R A C T The renal response to chronic depletion of extracellular volume was examined using the techniques of micropuncture. Depletion of salt and water was produced by administration of furosemide to rats maintained on a sodium-free diet. There was a marked fall in body weight, plasma volume, and glomerular filtration rate. The intrinsic reabsorptive capacity of the proximal tubule, measured by the split-droplet technique, was greatly enhanced. The acceleration of proximal fluid reabsorption could not be accounted for by changes in filtration rate, tubular geometry, or aldosterone secretion. The half-time of droplet reabsorption in the distal tubule was not altered by sodium depletion.An increase in the reabsorption of fluid in the proximal tubule, as demonstrated directly in the present experiments, provides an explanation for a variety of clinical phenomena associated with volume depletion. INTRODUCTIONIt is now well established that expansion of the extracellular fluid leads to renal excretion of salt and water in large part through the mechanism of decreased reabsorption in the proximal tubule. It is also well-known that depletion of extracellular volume regularly induces retention of salt and water, but the mechanism is not so precisely established. There is reason to think that, in addition to a fall in glomerular filtration rate, there is an accelerated reabsorption of sodium in the proximal tubules resulting in decreased delivery of filtrate to the distal nephron. Thus far, however, the evidence has been