Flow of capillary fluid and interstitial fluid in the kidney
Two factors determining renal tubular reabsorption directly affected by hemodynamic changes in the kidney are the hydrostatic osmotic pressure and colloid of the tubular capillaries.
Because of the importance of maintaining an accurate balance between glomerular filtration and tubular reabsorption, many nerves, hormones and local mechanisms are involved in the regulation of reuptake. absorption of the renal tubules as well as glomerular filtration. The most striking importance of reabsorption is that the reabsorption of some substances can occur independently of others, especially in the presence of hormones.
The hydrostatic and colloidal forces govern the rate of reabsorption across the peritoneal capillaries, just as they control filtration in the glomerular capillaries.
Changes in glomerular capillary reabsorption can affect the hydrostatic and colloidal pressure of the renal interstitial and ultimately the renal tubular reabsorption of water and solutes.
The normal value of flow rate and reabsorption rate
When glomerular filtrate passes through the renal tubules, more than 99% of water and most dissolved substances are reabsorbed normally. The fluid and electrolytes are reabsorbed from the tube into the renal interstitial and from there into the renal tubular capillaries.
The normal rate of renal tubular capillary reabsorption is approximately 124 ml/min.
The reabsorption through the tubular capillaries may be calculated as follows:
The amount of reabsorption = Kf x the reabsorption pressure
The net reabsorption force represents the sum of the hydrostatic and colloidal forces that are beneficial to or against reabsorption through the tubular capillaries.
These forces include (1) hydrostatic pressure inside the tubular capillaries (hydrostatic pressure around the tubule [Pc]), against reabsorption; (2) hydrostatic pressure in the renal cavity (Pif) outside the capillary, assists with reabsorption; (3) colloidal osmotic pressure of renal tubular capillary plasma protein (πc), assists with reabsorption; and (4) colloidal osmotic pressure of interstitial proteins (πif), against reabsorption.
Figure. Summary of hydrostatic forces and colloidal pressure determine the process of reabsorption into the capillary lumen around the renal tubule.
The figure shows the approximate normal forces that are beneficial and counteract the renal tubular capillary reabsorption. Because the normal pressure of the tubular capillaries averages about 13 mm Hg and the renal interstitial hydrostatic pressure averages 6 mm Hg, there is a positive hydrostatic pressure gradient from the peritoneal capillary to the interstitial fluid about 7 mm Hg. , against fluid reabsorption. This opposition to fluid reabsorption rather than counterbalance because the osmotic pressure of the colloid is conducive to reabsorption. The plasma colloidal osmolality, which aids reabsorption, is about 32 mm Hg, and the interstitial colloid osmotic pressure, against reabsorption, is 15 mm Hg, causing a net colloidal osmolality of about 17 mm Hg, conducive to reabsorption. Therefore, subtracting the net hydrostatic forces against reabsorption (7 mm Hg) for the net colloidal osmotic forces conducive to the reabsorption (17 mm Hg) gives a net reabsorption force of about 10 mm Hg. . This value is high, similar to that found in glomerular capillaries, but in the opposite direction.
Another factor that contributes to the high rate of fluid reabsorption in the tubular capillaries is the large filtration coefficient (Kf) because of the high hydraulic conductivity and the large surface area of the capillaries. Because the normal rate of reabsorption is about 124 ml/min and the net reabsorption pressure is 10 mm Hg, the normal Kf is about 12.4 ml/min / mm Hg.
Regulates renal tubular capillary flow
Two factors determining renal tubular reabsorption directly affected by hemodynamic changes in the kidney are the hydrostatic osmotic pressure and the colloid of the tubular capillaries. The renal tubular capillary hydrostatic pressure is influenced by the artery pressure and the resistance of the inward and outward arterioles as follows. (1) Increased arterial pressure tends to increase peritoneal capillary hydrostatic pressure and decrease the rate of reabsorption. This effect is buffered to some extent by the self-regulation mechanism that maintains a relatively constant blood flow to the kidney, as well as a relatively constant hydrostatic pressure in the renal vascular. (2) An increase in resistance of the radial or outward arterioles reduces the renal tubular capillary hydrostatic pressure and tends to speed up reabsorption.
Although contraction of the outflow of arterioles increases glomerular capillary hydrostatic pressure, it reduces peritoneal capillary hydrostatic pressure.
The second major determinant of renal tubular capillary reabsorption is the colloidal osmotic pressure of the plasma in these capillaries; Elevated the osmotic pressure of the colloid increases the reabsorption in the renal tubular capillaries. The colloidal osmotic pressure of the tubular capillary is determined by (1) the systemic plasma colloid osmolality (the higher the plasma protein concentration of the filtered system blood, the greater the glomerular filtration fraction) and therefore, the more concentrated the protein is in the remaining plasma).
Consequently, an increase in filtration also tends to speed up renal tubular capillary reabsorption.
Since filtration is defined as the GFR / RPF ratio, an increased filtration may be due to an increase in GFR or a decrease in RPF. Some renal vasoconstrictors, such as angiotensin II, increase renal tubular capillary reabsorption by decreasing RPF and increasing filtration.
Changes in the renal tubular capillary Kf can also affect the rate of reabsorption since Kf is a measure of the permeability and surface area of the capillaries. An increase in Kf increases reabsorption, while a decrease in Kf decreases renal tubular capillary reabsorption. Kf is constant under most physiological conditions.
Board. Factors that affect renal tubular capillary reabsorption.
Hydrostatic and colloidal osmotic pressure in the interstitial kidney
Finally, changes in the physical force of the tubular capillaries affect tubular reabsorption by varying the physical forces in the interstitial renal tubules. For example, a decrease in the renal tubular capillary reabsorption force due to an increase in renal tubular capillary hydrostatic pressure or a decrease in the colloid osmotic pressure of the tubular capillary reduces the uptake of interstitial fluids and solutes. into the renal tubular capillaries. This action in turn increases the hydrostatic pressure of the renal interstitial fluid and reduces the osmotic pressure of the interstitial fluid due to dilution of the interstitial proteins. These changes then reduce the net reabsorption of fluid from the renal tubules to the interstitial, especially in the proximal tubules.
The mechanism by which interstitial fluid hydrostatic pressure and colloidal osmolality affect tubular reabsorption is understood by considering the pathways by which solute and water are reabsorbed. Once solutes enter the intercellular or interstitial channels by either active transport or passive diffusion, water is drawn from the lumen into the interstitial by osmosis. Furthermore, once water and dissolved substances are in the interstitial space, they can either be caught up in the tubular capillaries or diffused back through the epithelial junctions into the lumen. The so-called "tight" junction between the epithelial cells of the proximal tubule actually leaks, so a significant amount of sodium can diffuse in both directions through these junctions. With a normally high rate of renal tubular capillary reabsorption, the net movement of water and dissolved substances into the tubular capillaries of the renal tubules with less penetration into the lumen. However, when tubular capillary reabsorption is reduced, the interstitial hydrostatic pressure increases and there is a tendency for a greater amount of solute and water to seep back into the lumen, thereby reducing the rate of reabsorption real.
The reverse is true when renal tubular capillary reabsorption increases above normal levels. The initial increase in reabsorption by the tubular capillaries tends to decrease the hydrostatic pressure of the interstitial fluid and increase the osmotic pressure of the interstitial colloid. Both of these forces are conducive to the movement of fluid and solute out of the lumen and into the interstitial; as a result, water and solutes residue in the lumen decreases, and net reabsorption in the tubules increases.
Consequently, through the hydrostatic and colloidal changes of the renal wall, the renal tubular capillary uptake of water and solutes coincides with the net reabsorption of water and solutes from the tubular lumen. into the interstitial kidney. In general, forces that increase renal tubular reabsorption also increase renal tubular reabsorption.
In contrast, hemodynamic changes that inhibit peritoneal capillary reabsorption also inhibit renal tubular solute and water reabsorption.