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Ch 28 - Urine Concentration and Dilution, Regulation of ECF

Terms in this set (39)

1 - assume the loop of henle is filled with fluid at a concentration of 300 (same as proximal tubule)

2 - the active ion pump of the TAL reduces the concentration inside the tubule and raises the interstitial concentration. the limit to the gradient is 200 because paracellular diffusion of inos back into the tubule eventually counterbalances transport of ions out of the lumen when the gradient is achieved

3 - the tubular fluid of the TDL and the interstitial fluid quickly reach osmotic equilibrium because of osmosis out of the descending limb. Interstitial osmolarity is maintained at 400 because of continued transport of ions out of the thick ascending limb

4 - additional flow of fluid into the loop of henle from the proximal tubule which causes the hyperosmotic fluid previously formed in the descending limb to flow into the ascending limb.

5 - 200 mosm gradient is established

6- fluid in the descending limb reaches equilibrium with the hyperosmotic medullary interstitial fluid

These steps are repeated over and over with the net effect of adding more and more solute to the medulla in excess of water, with sufficient time, this process gradually traps solutes in the medulla and multiplies the concentration gradient established by the active pumping of ions out of the TAL, eventually raising the interstitial fluid osmolarity to 1200

Thus the repetitive reabsorption of sodium chloride by TAL and continued inflow of new sodium chloride from the proximal tubule into the loop of Henle is called the countercurrent multiplier
A healthy person usually excretes about 20-50% of the filtered load of urea.

Urea excretion rate controlled by
- concentration of urea in the plasma
- glomerular filtration rate

In the proximal tubule, 40-50% of the filtered urea load is absorbed, but the tubular fluid urea concentration increases because urea is not nearly as permeable as water. There is some secretion of urea into the thin loop of henle from the medullary renal interstitium by UTA-2

Thick AL, DCT, CT are impermeable to urea

When the kidney is forming concentrated urine and high levels of ADH are present, reabsorption of water from distal tubule and cortical collecting tubule further raises the tubular fluid concentration of urea. As this urea flows into the inner medullary collecting duct, the high tubular fluid concentration of urea and specific urea transporters (UTA3) cause urea to diffuse into the medullary interstitum

Moderate amount of the urea in the medullary intersitium eventually diffuses into the thin loop of henle and diffuses upward as a recycling process.

this urea circulation provides an additional mechanism for forming a hyperosmotic renal medulla

when there is excess water in the body, urine flow rate is usually increased and therefore the concentration of urea in the inner medullary collecting ducts is reduced causing less diffusion of urea into the renal medullary interstitium. ADH levels are also reduced when there is excess body water and this in turn decreases the permeability of the inner medullary collecting ducts to urea and water
W/o a special medullary blood flow system, the solutes pumped into the renal medulla by the counter current multiplier system would be rapidly dissipated
- Medullary blood flow is low, accounting for less than 5% of the total renal blood flow. This sluggish blood flow is sufficient to supply the metabolic needs of tissues but helps to minimize solute loss from the medulary interstitium
- Vasa recta serve as countercurrent exchangers, minimizing washout of solutes from the medullary interstititum

Blood enters and leaves the medulla by way of the vasa recta at the boundary of the cortex and medulla, highly permeable to solutes

As blood descends into the medulla toward the papillae, it becomes progressively more concentrated partly by solute entry from interstitium and loss of water. (1200 osmo)

As the blood ascends back toward the cortex,it becomes progressively less concentrated as solutes diffuse back out into the medullary interstitium and as water moves into the vasa recta

Although there are large amounts of fluid and solute exchange across the vasa recta, there is little net dilution of the concentration of the interstitial fluid at each level of the renal medulla because of the U shape of the vasa recta capillaries, which act as counter current exchangers

Thus the vasa recta do not create the medullary hyperosmolarity, but they do prevent it from being dissipated

Under steady state conditions, the vasa recta carry only as much solute and water as is absorbed from the medullary tubules and the high concetration of solutes established by the counter current mechanism is preserved
When sodium intake is low, increased levels of these hormones stimulate sodium absorption by the kidney and therefore prevent large sodium losses, even though sodium intake may be reduced to as low as 1o percent of normal

Although these hormones increase the amount of sodium in the ECF, they also increase the ECF volume by increasing reabsorption of water along with the sodium. Therefore AT II and aldosterone have little effect on soidum concentration, except under supreme conditions

Two main reasons why changes in angiotensin and aldosterone do not have a major effect on plasma concentration.
- Angiotensin and aldosteroe increase both sodium and water reabsorption by the renal tubules, leading to increased in ECF volume and sodium quantity but little change in sodium concentration
- As long as the ADH thirst mechanism is functional, any tendency toward increased plasma sodium concentration is compensated for by increased water intake or increased plasma ADH secretion, which tends to dilute the ECF back toward normal

Even in patients with primary aldosteronism, who have extremely high levels of aldosterone, the plasma sodium concentration usually increases only about 3-5 meq/L

Addisons Disease - One of the reasons for the large losses of sodium eventually cause severe volume depletion and decreased blood pressure, which can activate the thirst mechanism through the cardiovascular reflexes. This leads to a further dilution of the plasma sodium concentration, even though the increased water intake helps to minimize the decrease in body fluid volumes under these conditions.

Even so the ADH thirst mechanism is by far the most powerful mechanism for controlling ECF osmolarity and sodium concentration