distal tubule

Damage to the distal tubule may cause loss of urine-concentrating ability and polyuria.

Additionally, it increases the secretion of potassium in the distal tubule and collecting ducts.

Sodium absorption by the distal tubule is mediated by the hormone aldosterone.

Thiazide diuretics also increase calcium reabsorption at the distal tubule.

Macula densa cells are columnar epithelium thickening of the distal tubule.

There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.

This hormone stimulates the reabsorption of sodium ions from distal tubules and collecting ducts.

It is secreted in response to increased mean arterial pressure and increased blood volume from the cells of the distal tubule and collecting duct.

Because of this increased absorption, less NaCl is present at the distal tubule where the macula densa is located.

Trichlormethiazide works by inhibiting Na/Cl ion reabsorption from the distal tubules of the kidneys.

The distal tubules of the kidneys secrete large amounts of uromucoid (Tamm-Horsfall protein).

This occurs through insertion of water channels (Aquaporin-2) into the apical membrane of distal tubule and collecting duct epithelial cells.

Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late distal tubule of the nephron.

Low levels of aldosterone stimulation of the renal distal tubule leads to sodium wasting in the urine and H+ retention in the serum.

The kidney: Here the brush border is useful in distinguishing the proximal tubule (which possesses the brush border) from the distal tubule (which does not).

In the kidneys, probenecid is filtered at the glomerulus, secreted in the proximal tubule and reabsorbed in the distal tubule.

The close proximity and prominence of the nuclei cause this segment of the distal tubule wall to appear darker in microscopic preparations, hence the name macula densa.

Trimethoprim antagonises the epithelial sodium channel (ENaC) in the distal tubule, thus acting like amiloride, this can cause hyperkalemia.

Additionally, increased aldosterone secretion causes increased distal tubule K secretion, in turn causing the hypokalemia seen with contraction alkalosis.

Trials of PRC200-SS in cynomolgus monkeys showed dose proportional kidney toxicity, with signs that the compound was damaging to the distal tubule and collecting duct.

The hypodynamic state is usually seen early in adrenal insufficiency and is associated with volume depletion from diarrhea, vomiting, and decreased reabsorption of sodium in the distal tubule.

Aldosterone has effects on most or all cells of the body but, clinically, the most important actions are on cells of the late distal tubule and medullary collecting duct.

Increasing the water permeability of distal tubule and collecting duct cells in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis.

This has led some observers to describe the lumen of proximal tubules as occluded or "dirty-looking," in contrast to the "clean" appearance of distal tubules, which have quite different properties.

Metabolic acidosis (increased blood acidity), also is due to loss of the hormone aldosterone because sodium reabsorption in the distal tubule is linked with acid/hydrogen ion (H+) secretion.