Distal Convoluted Tubules Overview

The initial part of the Distal Convoluted Tubule (DCT) is similar to the thick segment of the ascending loop of Henle.

The initial part of the DCT is relatively impermeable to water and solutes like urea, sodium, and chloride.

The initial DCT reabsorbs sodium by primary active transport, and chloride follows passively.

The initial part of the DCT secretes hydrogen ions mainly by secondary active transport.

The late DCT reabsorbs sodium, calcium, and chloride while also secreting hydrogen and buffers.

Sodium reabsorption in the late DCT is primarily regulated by aldosterone hormone.

Calcium reabsorption in the late DCT is regulated by parathyroid hormone.

The late DCT uses intercalated cells to secrete hydrogen ions independently of sodium, using primary active transport.

Urea is passively reabsorbed in the inner part of the medullary collecting ducts (CDs) because these parts are partially permeable to it, especially in presence of ADH. Urea is not reabsorbed in the cortical CDs and outer medullary CDs due to their impermeability to urea.

Water reabsorption in the CDs is regulated by ADH. In the absence of ADH, the CDs are impermeable to water. With ADH, the CDs become permeable to water due to activation of aquaporins.

Facultative water reabsorption refers to the variable water reabsorption in the collecting ducts and DCT, depending on the level of ADH.

The cortical CDs receive hypotonic tubular fluid from the DCTs. At normal ADH levels, about 10% of filtered water is reabsorbed passively, making the fluid isotonic at the end of the cortical CDs.

Medullary CDs receive isotonic fluid from the cortical CDs. This fluid is further reabsorbed by the hyperosmotic medullary interstitium, leading to an additional 4.7% of water reabsorption.

The secretion of potassium ions ($K^+$) occurs in the cortical CDs in exchange for sodium reabsorption. This process is increased by the aldosterone hormone.

Hydrogen ions ($H^+$) are secreted throughout the CDs by both active and passive mechanisms. Cortical CDs use both primary and secondary active transport, while medullary CDs mainly use primary active transport.

Buffers are secreted in the CDs like in the DCTs.

The process of increasing urine output.

This type of diuresis is triggered by drinking a lot of water, increasing urine volume.

Caused by substances that don't readily get absorbed in the proximal convoluted tubule, leading to more fluid excretion.

When the blood is too concentrated (hypertonic), ADH levels go UP, making the collecting ducts more permeable to water, leading to concentrated urine.

When the blood is too dilute (hypotonic), ADH levels go DOWN, making the collecting ducts less permeable to water, resulting in diluted urine.

A mechanism where both potassium and hydrogen ions ($K^+$ and H$^+$) compete for secretion by the distal convoluted tubules (DCTs) and cortical collecting ducts.

The process of excreting potassium ions (K$^+$) into the urine through the active transport of K$^+$ from the tubular cell into the tubular lumen.

The process of urine acidification occurs through the secretion of hydrogen ions (H$^+$) into the tubular lumen mainly in the proximal convoluted tubules (PCTs), distal convoluted tubules (DCTs) and collecting ducts.

The process by which the kidneys use specialized cells called intercalated cells to actively transport hydrogen ions (H$^+$) against their concentration gradient, into the tubular lumen.

The buffer system that is more effective in the tubular fluid than in the blood due to its high concentration within the urine.

This buffer system is composed of the weak base ammonia (NH$_3$) and its conjugated acid ammonium ion (NH$_4^+$).

The process by which the kidneys control the composition of the urine in the collecting ducts, primarily by regulating the reabsorption of sodium, water and the secretion of potassium.

This part of the collecting duct is responsible for fine-tuning the urine composition by regulating the final reabsorption of sodium (Na$^+$), water, and the excretion of potassium into the urine.