Saturday, December 13, 2008

Kidney Function Animation

As everyone knows we have two kidneys, each functioning independently, Diuretic action occurs in the kidney this is where the body controls the fitration,reabsorption and excretion of water small molecules and ions such as sodium and potassium .Outer layer if the kidney is called cortex, and the inner layer is called Medulla which has millions of special structures called Nephrons.

Fitration and Excretion in the Nephron
Nephron is a tubular structure similar to pores pipe,Glomerules is the starting point for the flow through the nephron.Blood enters to Glomerules through Afferent arteriole blood exits the Glomerules to efferent arteriole.the blood is filtered in Glomerules by osmosis and diffusion.

As blood passes through the porous capillary loops water and small molecules (50,000 molecular weight) are filtered passing it to the Bowmanns space, this creates the luminal fluid flowing through the nephron tubule .

* About 1/5 of the total blood volume is continually filtered into the Bowmanns capsule.99% of this volume is reabsorb leaving only a small volume to be excreted as urine .
* Each section of the nephron has a different morphology of cells making up the single cell wall, which causes differences in water permeability and ion transport.
* First section of the nephron is called the proximal convoluted tubule; the proximal convoluted tubule is highly permeable.
* Capillaries nearby the proximal convoluted tubule absorbs about 65% filtered sodium and water. Which was let out by tubule.
* All diuretics called carbonic anhydrase inhibitors mostly act on this portion of the nephron.
* Proximal convoluted tubule leads into the Henle loop, which has a thin descending limb and thin and thick ascending limb. The thick ascending limb normally reabsorbs about 25% of filtered sodium but does not allow water to reabsorb.
* Sodium potassium chloride ion co-transporters are block by loop diuretics on the luminal membrane.
* Next section is called Distal Convoluted tubule; this section doesn't allow water to reabsorb but reabsorbs sodium from sodium chloride ion co-transporters.
* Thiazide diuretics act here on this transporter, the last section of the nephron is called collecting tubule. Sodium channel blockers and aldosterone antagonist diuretics act here.

Detail view
Re-absorption molecules
Each site on the nephron tubule, certain molecules are able to permeate the wall and leak out into the interstitium, these molecules will be reabsorb to the Para tubular capillary and will be returned to the systemic blood supply

Inside tubule
As tubule wall is made-up of single layer cells, water molecules flow through the tubule

Loop of Henle and Loop Diuretics

* The sodium potassium ATPase transporter drives sodium reabsorption on the antiluminal membrane.
* For every 3 Sodium ions moving out of the cell to the interstitium 2 Potassium ions move from the interstitium to the cell. This causes a deficit of the sodium within the cell. The sodium potassium chloride transporter on the luminal membrane of the cell makes up this deficit. This transporter moves 1 Sodium, 1 Potassium, and 2 Chloride ions from the lumen into the wall of the nephron.
* Two potassium and chloride ions move down the concentration gradients to their respective channels.
* The potassium returns to the lumen through a potassium channel. The chloride is removed to the interstitium through chloride channel. The net result is a continuing transport of 3 Sodium ions and 6 Chloride ions from the luminal fluid into the interstitium. This sodium is reabsorb into the circulation.
* Because of the secretion of potassium a positive voltage is generated in the lumen resulting in re-absorption of possibly charged ions to the paracellulary Junction
* Loop Diuretics -Blockage of Na+,K+,Cl- transporter
* When the loop diuretics block the sodium potassium chloride transporter the sodium potassium exchange begins.
* The sodium from the lumen cannot replace sodium deficit. This blocks the overall re-absorption of sodium from this site and the nephron.
* The net result is greater excretion of sodium chloride potassium calcium and magnesium in the presence of the loop diuretics.

Distal Convoluted Tubule Thiazide diuretics

* Transporters present in the distal convoluted tubule are slightly different than those described in the ascending limb. in the distal convoluted tubule the sodium chloride Co- transporter replaces the sodium deficit caused by the sodium potassium ATPase.
* The chloride is reabsorb through chloride channels and the potassium returns to the interstitium through potassium channel.

Distal Convoluted Tubules
However the thiazide diuretics bind that the chloride binding site and block the sodium chloride Co. transporter. This blocks sodium and chloride re-absorption resulting in next excretion of sodium and chloride.

Collecting Tubule sodium channels inhibitors (Na+)

Transporters present in the collecting tubules are slightly different than at the other sites of the nephron, sodium potassium exchange occurs on anti-luminal membrane, however the sodium is replaced at this site are the sodium channels on the luminal membrane and potassium excretion is completed by transport through potassium channels on the luminal membrane. this continuing exchange results in overall sodium re-absorption and potassium excretion .

When the sodium channel inhibitors are present they block the sodium channel, this prevents the continual re-absorption of sodium and also prevents the overall excretion of potassium this is why sodium channel inhibitors are called potassium sparing.
Thus all the diuretic agents described directly decrease the re-absorption of sodium by blocking specific ion transporters in the various segments of the nephron tubule this indirectly affects re-absorption and excretion of water and other ions as described for each type of diuretic

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