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 Fluid exchange across capillaries  

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For some reason, i can never understand this concept, can somenone please help.Why would an increase in Interstitial fluid oncotic pressure favor filtration and an increase in oncotic capillary pressure oppose filtration?


this is long but maybe helpful


A. The initial event in urine formation is the production of an ultra-filtrate whose concentrations of water and freely filtered ions and molecules are almost identical to those of plasma. About 125 ml/min of fluid is filtered from about 700 ml/min of plasma flowing into the kidney.

B. The components of the glomerular filtration barrier are: (1) the endothelial cells of the glomerular capillaries; (2) the capillary basement membrane, and (3) the filtration slits of the foot processes of the podocytes of Bowman's capsule that invest the "underside" of the glomerular basement membrane.

1. The endothelial cells. The fenestrations between the glomerular endothelial cells are about 700 Å wide. Thus they prevent the passage of cells, but not of macromolecules.

2. The glomerular basement membrane is an important component of the filtration barrier. It prevents the filtration of large plasma proteins (70 to 100 Å in radius) and retards the passage of smaller plasma proteins.

3. The podocyte foot processes are the final and finest filtration barrier. The fenestrations between the foot processes are bridged by a thin membrane containing small rectangular filtration slits that are about 40Å x by 140 Å. The filtration slits prevent the filtration of all but small proteins.

4. The role of electrical charge. The membranes of all three components of the filtration barrier contain glycoproteins, whose sialic acid moieties bear a negative charge that repels negatively charged macromolecules from the filtration barrier. Thus negatively charged macromolecules, such as most plasma proteins, are more effectively excluded from filtration than are neutral or cationic molecules.

5. Glomerular filtration of molecules depends on their molecular size. The concentration of serum albumin in the glomerular filtrate is much less than 0.01 of its plasma concentration. Nevertheless, because of the huge volume of plasma filtered (180 L/day), about 7 grams of albumin are filtered each day. The proximal tubular cells reabsorb almost all of this albumin, so that in healthy individuals the protein concentration in the urine approaches zero.

a. The radius of the hemoglobin molecule is about 32 Å and its filterability is 0.03. In cases of severe hemolysis, significant amounts of hemoglobin may appear in urine.

b. Myoglobin, radius 19.5 Å, released from muscle due to disease or trauma readily crosses the glomerular filtration barrier and may appear in urine.

C. The rate of glomerular filtration is determined by Starling forces.

1. The hydrostatic pressure in the glomerular capillary (PGC) and the oncotic pressure of the ultrafiltrate (p BS) favor filtration across the glomerular barrier. The hydrostatic pressure in Bowman's space (PBS) and the oncotic pressure in the glomerular capillary blood (p GC) oppose filtration. The net filtration pressure is

Pnet = PGC - p GC - PBS + p BS

2. The GFR is equal to the net driving force (Pnet) times the effective filtration coefficient (Kf) of the glomerular filtration barrier, which is equal to the hydraulic conductivity per cm2 area of the glomerular capillaries times the total area of the glomerular capillaries.

GFR = KfPnet = Kf (PGC - p GC - PBS + p BS)

The net filtration pressure in the glomerulus is similar to that in other capillary beds, but Kf is 50 to 100 times greater. The rate of filtration at the glomerulus is thus very high compared to other capillaries.

3. Components of the net filtration pressure Pnet

a. Removal of proteins by the glomerular barrier (sieving) reduces the protein concentration of the fluid in Bowman's space to near zero, so that the tubular oncotic pressure (p t ) » 0. Thus Pnet is approximately equal to PGC - p GC - PBS .

b. The glomerular capillary hydrostatic pressure, about 45 mm Hg, does not change much as blood flows through the glomerular capillaries. The largest pressure drops in the renal circulation occur across the afferent and efferent arterioles.

c. The hydrostatic pressure in Bowman's space is about 10 mm Hg.

d. The oncotic pressure of plasma is about 25 mm Hg

e. Thus at the beginning of the glomerular capillary

Pnet = PGC - p GC - PBS = 45 - 25 -10 = 10 mm Hg

f. As plasma flows through the glomerular capillaries, water is filtered into Bowman's space, but protein remains. Thus the protein concentration and the oncotic pressure of plasma increase along the glomerular capillary. If p GC were to rise by 10 mm Hg, net filtration would cease. Using the value above, if FF = 0.20, then Pnet would fall to 3.75 mm Hg by the end of the glomerular capillary.

D. Regulation of the rate of glomerular filtration. Physiological regulation of GFR occurs via alterations in Pnet (via changes in PGC or p GC) or by changes in Kf .

1. The most common means of altering Pnet and hence GFR is by changes in the glomerular hydrostatic pressure (PGC). Suppose that in a dehydrated individual Pnet falls from 45 mm Hg to 40 mm Hg. This would cause the net filtration pressure to drop from 10 to 5 mm Hg and the GFR to drop to half the normal value. PGC (and thus GFR) is controlled by the activities of the afferent and efferent renal arterioles. Constriction of the afferent arteriole or dilation of the efferent arteriole will reduce PGC. Dilation of the afferent arteriole or constriction of the efferent arteriole will increase PGC.

2. Net GFR is dependent on the flow rate in glomerular capillaries. If the flow rate is increased in glomerular capillaries, with a constant GFR at the beginning of the capillary, blood must flow along a greater length of glomerular capillary before the oncotic pressure rises enough to slow net filtration to a given extent. In this way the average plasma oncotic pressure in the glomerular capillaries will determine the net GFR. The total GFR will thus increase with increased flow rate. Decreased blood flow rate will result in the oncotic pressure rising more rapidly along the glomerular capillary and result in diminished overall GFR.

3. GFR may be reduced by increased activity in renal sympathetic nerves. Sympathetic impulses constrict both afferent and efferent arterioles and thus decrease renal blood flow, while having relatively little effect on PGC. Due to the decrease in glomerular blood flow, there is a decrease in GFR via the mechanism just described in point 2.

4. GFR may be changed by alterations in Kf. This occurs physiologically and in diseases.

a. Kf can be decreased by contraction of the mesangial cells that surround the glomerular capillaries. When mesangial cells contract, some of the glomerular capillaries are closed or their flow is reduced. Angiotensin II causes both a reduction in flow by constricting efferent arteriolar smooth muscle, and a reduction in Kf by closing capillaries by means of mesangial contraction.

b. Glomerular permeability changes are an important part of the etiology of a number of clinical syndromes, e.g., antigen- antibody reactions secondary to systemic infections. This can involve destruction of glycoproteins in the filtration barrier, thus diminishing the net negative charge in the filtration barrier, resulting in proteinuria. In other instances, inflammatory processes may damage the filtration barrier and result in a dramatic decrease in Kf. Prostaglandin E1, acetylcholine, and bradykinin have all been shown to be capable of reducing Kf, although they are vasodilators.


oh my god dxtxpx!!!!!
good explanation, but for your sake i hope rida asked about the glomerular capillaries and not about general tissue capillaries, as i first thought.... :lol: :lol:

anyway, your great effort should be appreciated!!! :wink:


WOW, thank you so much dxtxpx, I really appreciate it, just like anne said.... :o)


oops, I mean Alina, sorry!!!


So general capillaries work differently??


well its not like i typed it myself, just cut and paste. i was reading this for myself and since rida asked the question, i pasted it here. yeah alina u r right, i dont even know if rida asked specifically for renal capillaries but thats what i was studying :?


well general principal is the same: Sterling Equation
here is a colorful site link


to tell the truth , i havent had the patience to read the post :lol: :lol:

basically, the mechanism is this:
oncotic pressure is given mostly by protein concentration and its one of the factors that influence fluid exchange between capillaries and interstitium. (the other one is hydrostatic pressure). an increase in oncotic presure on either side will attract fluid, to balance the pressure gradient.
so, an increase in interstitial oncotic pressure will determine water to come into the interstitium from the blood = increase in filtration. and viceversa.
hydrostatic pressure works the other way around: an increase in interstitial hydr press determines fluid to go into the capillary , thus decrease in filtration.

did i make it clear enough? :lol:


simple and effective grin grin


couldn't be more clear!!! THANX GUYS!

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