Functions of the Distal Convoluted Tubules (DCTs) - PDF
Document Details
Uploaded by SelfSufficiencySplendor
Tags
Summary
This document presents an overview of the functions of the distal convoluted tubules (DCTs) in the human kidney and the role of various transport mechanisms involved in urine formation. The mechanisms of acidification of urine through the secretion of hydrogen ions and the role of buffer systems are also described.
Full Transcript
# Functions of the Distal Convoluted Tubules (DCTs) - The DCTs receive hypotonic fluid from the ascending limbs of the loops of Henle. - Functionally, they are divided into two parts: - **The initial part:** - Has the same characteristics as the thick segment of the ascending limbs of l...
# Functions of the Distal Convoluted Tubules (DCTs) - The DCTs receive hypotonic fluid from the ascending limbs of the loops of Henle. - Functionally, they are divided into two parts: - **The initial part:** - Has the same characteristics as the thick segment of the ascending limbs of loop of Henle. - Is almost impermeable to both water and solutes (urea, $Na^+$ and Cl). - $Na^+$ is reabsorbed by primary active transport, and Cl follows it passively. - The tubular fluid becomes more hypotonic (about 100 mOsm/liter). - This part is called the diluting segment of the nephron. - The initial parts of DCTs secrete $H^+$ mainly by secondary active transport. - **The late part:** - Performs the following functions: - **Reabsorption:** - $Na^+$ reabsorption: - Occurs by primary active transport. - Is controlled mainly by aldosterone hormone. - Is followed by passive reabsorption of Cl and water. - About only 5% of the filtered water is reabsorbed in the DCTs as they are poorly permeable to water. - There is no urea reabsorption because the DCTs are normally poorly permeable to urea. - The fluid delivered from the DCTs into the collecting ducts is hypotonic. - $Ca^{++}$ reabsorption: - Also occurs by primary active transport. - Increased by the parathyroid hormone. - **Secretion:** - $H^+$ secretion: - Occurs mainly by secondary active transport by $Na^+-H^+$ antiport carrier. - However, certain cells called intercalated, dark or brown cells start to appear in this segment (and become more abundant in the collecting ducts). - These cells secrete $H^+$ independent of $Na^+$(by primary active transport) against high concentration gradient by specific uniport carrier protein and $H^+-ATPase$. - **Secretion of buffers for excess $H^+$ in the DCTs:** - The kidney often excretes urine at pH as low as 4.5 in acidosis or as high as 8 in alkalosis. - In acidosis, the urine is buffered by the following buffer systems to prevent marked decrease of pH below 4.5: - **Bicarbonate buffer:** - $HCO_3^-$ ions and $H^+$ are normally titrate each other in the tubules mainly in the PCTs. - The remaining excess $H^+$ in the tubular fluid is buffered by the phosphate and ammonia buffers. - **Phosphate buffer:** - This buffer is much more powerful in the tubular fluid than in blood (due to its high concentration in the urine). - **Ammonia buffer** - $K^+$ secretion: - Occurs actively as follows: - $K^+$ is transported inside the tubular cells by the $Na^+-K^+$ pump at their basolateral borders. - Then, it is secreted by counter-transport mechanism at their luminal borders of the principle cells (which start to appear in this segment), into the tubular fluid in exchange for $Na^+$ reabsorption (utilizing an antiport carrier). - $K^+$ secretion in the DCTs and cortical collecting ducts is increased by: - Increase the extracellular $K^+$ level. - Increase aldosterone level. - $K^+$ and $H^+$ compete for secretion in the DCTs and cortical collecting ducts. - An increase of any of these ions in the tubular cells favors its secretion. # Acidification of Urine ($H^+$ Secretion) by the Renal Tubules - Urine acidification occurs by secretion of $H^+$ into the tubular lumen. - This mostly occurs in the PCTs, DCTs and collecting ducts. - To lesser extent in the ascending limbs of loop of Henle. - It occurs as following: - $H^+$ is formed inside the renal tubular cells as a result of dissociation of $H_2CO_3$ (The later is formed by combination of $CO_2$ and $H_2O$ under the influence of C.A enzyme). - Then $H^+$ is secreted by either: - **Secondary active transport:** - In exchange for $Na^+$ reabsorption (i.e., by counter-transport utilizing an antiport carrier). - It occurs in the PCTs, loop of Henle, DCTs, and collecting ducts. - **Primary active transport:** - This occurs against high $H^+$ concentration gradient by the intercalated cells. - These cells are abundant in the late parts of the DCTs and the collecting ducts. - It occurs only in the late DCTs and collecting tubules. # Functions of the Collecting Ducts (CTs) - The collecting ducts receive hypotonic fluid from the DCTs. - Functionally, they are divided into two parts: - Cortical part. - Medullary part. - They perform the following functions: - **Reabsorption:** - $Na^+$ reabsorption: - This occurs by primary active transport all over the CDs. - It increases by aldosterone only in the cortical CDs. - It is followed by passive diffusion of Cl and water. - It is coupled with $K^+$ secretion. - Urea reabsorption: - This occurs by passive diffusion only in the inner parts of the medullary CDs (because these parts are partially permeable to urea), especially in the presence of ADH. - Urea is not reabsorbed in both cortical CDs and the outer parts of medullary CDs (because these parts are impermeable to urea). - Water reabsorption in the CDs: - The CDs are relatively impermeable to water in absence of ADH. - However, in the presence of ADH the CDs become highly permeable to water (due to activation of water channels in that segment which are called aquaporins [AQP2 and AQP3]). - Water reabsorption in the CDs and to some extent also in the DCTs is called facultative water reabsorption (because it depends on the blood level of ADH). - Water reabsorption in the cortical CDs occurs as following: - The cortical CDs receive hypotonic fluid from the DCTs. - At the normal rate of ADH secretion - about 10% of the filtered water is passively reabsorbed into the iso-osmotic cortical interstitium in excess of $Na^+$ reabsorption. - So, the tubular fluid becomes isotonic at the end of the cortical CDs. - Water reabsorption in the medullary CDs occurs as following: - This isotonic fluid enters the medullary CDs. - Then, an additional 4.7% of $H_2O$ is reabsorbed by the hyperosmotic medullary interstitium. - **Secretion** - $K^+$ secretion: - This occurs only in the cortical CDs in exchange for $Na^+$ reabsorption. - It is increased by the aldosterone hormone. - $H^+$ secretion: - It is secreted all over the CDs: - In the cortical CDs - it occurs by both primary and secondary active transport. - In the medullary CDs - it occurs mainly by primary active transport. - Secretion of buffers: As in DCTs. # N.B.1: Summary of Water Reabsorption Through the Different Parts of the Renal Tubules - Normally, about 99.7% of the filtered water is reabsorbed in the renal tubules as follows: - 65% in the PCTs. - 15% in the descending limb loop of Henle. - 5% in the DCTs. - 10% in the cortical CDs. - 4.7% in the medullary CDs. - Only 0.3% of the glomerular filtrations excreted producing about 1.5 liters urine daily with osmolarity about 400 mOsm/liter. # Urine Concentration and Dilution - **(1) Mechanism of urine concentration:** - This occurs in: - Hypovolemia (e.g., in dehydration and hemorrhage). - Blood hypertonicity (e.g., due to excessive salt intake). - This mechanism depends only on the facultative water reabsorption in the CDs which is determined by two main factors: - **Blood level of ADH:** - When it increases in (hypovolemia or hypertonicity) - increase the permeability for water reabsorption in the CDs and to the little extent the late part of DCTs. - Increase ADH secretion - larger part of the medullary CDs become water-permeable so, more water is reabsorbed resulting in excretion of concentrated urine. - **The hyperosmolarity of medullary interstitium:** - It is increased by countercurrent mechanism which causes passive diffusion of water from the CDs into the medulla. - The net effect is excretion of small volume of concentrated urine = (0.5 liter daily with an osmolarity about 1400 mOsm/liter). - **(2) Mechanism of urine dilution:** - This occurs in: - Hypervolemia. - Blood hypotonicity. - The following occurs: - **Inhibition of secretion ADH:** - This decreases the water permeability of the CDs - decrease the reabsorption of water. - **Decrease the osmolarity of medullary interstitium:** - The net effect is the excretion of large volume of diluted urine with an osmolarity less than 80 mOsm/liter. - e.g. in diabetes insipidus - complete absence of ADH - so, the urine volume 23.3 liter/day with osmolarity is about 30 mOsm/liter. # Diuresis - **Definitions** - Diuresis means increasing the rate of urine output. - **Types (methods of diuresis:** - **Water Diuresis:** - This is produced by drinking of a large amount of water which increases the urine volume after about 15 minutes. - The maximal diuresis occurs within 40-45 min. - While, the ingested amount is completely excreted after 2 hours. - **Osmotic diuresis:** - This is produced by administration of osmotically active substances that are not readily absorbed in the PCTs. - e.g. mannitol & sucrose. - **Difference between water and osmotic diuresis:** | | Water diuresis | Osmotic diuresis | |-----------------|------------------------------------------|---------------------------------------------------| | Water reabsorption | Facultative water reabsorption only ↓ | Obligatory & facultative water reabsorption are ↓ | | ADH secretion | Normal | Normal | | $Na^+$ excretion | Normal | ↑ | | Tonicity of urine | Hypotonic | Isotonic | - **Pressure diuresis:** - The changes in the ABP within the autoregulation level have a little effect on GFR with parallel changes in urine volume. - Marked increase in ABP - increase urine output. - Drop in the mean ABP below 50mmHg - stop urine formation.