Finally, the tubule dives back into the medulla as the collecting duct and then into the renal pelvis where it joins with other collecting ducts to exit the kidney as the ureter. It is important to note two things about this transporter. First, its activity is dependent on the tubular concentration of sodium, so that when sodium is high, more sodium is reabsorbed and more potassium and hydrogen ion are excreted.
Second, this transporter is regulated by aldosterone, which is a mineralocorticoid hormone secreted by the adrenal cortex. Increased aldosterone stimulates the reabsorption of sodium, which also increases the loss of potassium and hydrogen ion to the urine. Finally, water is reabsorbed in the collected duct through special pores that are regulated by antidiuretic hormone , which is released by the posterior pituitary.
ADH increases the permeability of the collecting duct to water, which leads to increased water reabsorption, a more concentrated urine and reduced urine outflow antidiuresis.
Diuretic drugs increase urine output by the kidney i. This is accomplished by altering how the kidney handles sodium. If the kidney excretes more sodium, then water excretion will also increase. Most diuretics produce diuresis by inhibiting the reabsorption of sodium at different segments of the renal tubular system. Sometimes a combination of two diuretics is given because this can be significantly more effective than either compound alone synergistic effect.
The reason for this is that one nephron segment can compensate for altered sodium reabsorption at another nephron segment; therefore, blocking multiple nephron sites significantly enhances efficacy.
Loop diuretics inhibit the sodium-potassium-chloride cotransporter in the thick ascending limb see above figure. This altered handling of sodium and water leads to both diuresis increased water loss and natriuresis increased sodium loss. By acting on the thick ascending limb, which handles a significant fraction of sodium reabsorption, loop diuretics are very powerful diuretics.
These drugs also induce renal synthesis of prostaglandins, which contributes to their renal action including the increase in renal blood flow and redistribution of renal cortical blood flow. Thiazide diuretics , which are the most commonly used diuretic, inhibit the sodium-chloride transporter in the distal tubule. Nevertheless, they are sufficiently powerful to satisfy many therapeutic needs requiring a diuretic.
Their mechanism depends on renal prostaglandin production. Because loop and thiazide diuretics increase sodium delivery to the distal segment of the distal tubule, this increases potassium loss potentially causing hypokalemia because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.
The increased hydrogen ion loss can lead to metabolic alkalosis. Part of the loss of potassium and hydrogen ion by loop and thiazide diuretics results from activation of the renin-angiotensin-aldosterone system that occurs because of reduced blood volume and arterial pressure.
Increased aldosterone stimulates sodium reabsorption and increases potassium and hydrogen ion excretion into the urine. There is a third class of diuretic that is referred to as potassium-sparing diuretics.
Unlike loop and thiazide diuretics, some of these drugs do not act directly on sodium transport. Some drugs in this class antagonize the actions of aldosterone aldosterone receptor antagonists at the distal segment of the distal tubule.
This causes more sodium and water to pass into the collecting duct and be excreted in the urine. Sheldon G. Sheps, M. There is a problem with information submitted for this request. Sign up for free, and stay up-to-date on research advancements, health tips and current health topics, like COVID, plus expert advice on managing your health. Error Email field is required. Error Include a valid email address. To provide you with the most relevant and helpful information and to understand which information is beneficial, we may combine your e-mail and website usage information with other information we have about you.
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Show references Mount DB. Causes of hypokalemia in adults. Accessed March 23, Types of blood pressure medications. American Heart Association. Bumetanide is 40 times more potent rapid diuresis than furosemide.
Torasemide Demadex : It has a more prolonged diuretic action than furosemide, with less potassium loss. No evidence of ototoxicity with torsemide use. Ethacrynic acid Edecrin : Non-sulfa drug other loop diuretics are sulfa drugs ; It is associated with greater side effects than other loop diuretics and is the most ototoxic loop diuretic , therefore its use is limited now.
It is used in patients hypersensitive to sulpha drugs. All loop diuretics have the same mechanism of action; however, they differ from each in pharmacokinetics. The absorption of loop diuretics is rapid with the peak serum concentration occurring within 0.
There is variability in the absorption of loop diuretics. Thus, switching from intravenous to oral route in those with lesser bioavailability such as furosemide requires higher oral doses than the IV dose. The route of elimination is mainly liver , in which they are metabolized by the cytochrome p enzyme. Sodium first binds to the cotransporter, promoting the binding of potassium and chloride ions, followed by binding with a second chloride ion.
License: CC BY 2. Table reference: PhilSchatz. This inhibitory effect of loop diuretics results in a decreased rate of sodium, chloride, potassium and other electrolytes reabsorption from these tubules into the medullary interstitium, thus inhibiting the formation of hypertonic medullary fluid. This leads to high osmotic pressure inside the renal tubules associated with a low osmolarity of the medullary interstitial fluid, which results in:.
An increased sodium excretion natriuresis and increased excretion of other electrolytes, such as chloride and potassium. Magnesium and calcium reabsorption is also inhibited because their absorption in the thick ascending limb depends mainly on the positive lumen voltage gradient , which is lost with loop diuretics usage. Thus, loop diuretics aims to increase sodium excretion from the body with a subsequent increase in urine output resulting in a decrease in the extracellular fluid ECF volume in the clinical conditions that are associated with extracellular fluid ECF expansion, such as hypertension and edema.
The inability of the heart to pump blood may result in pulmonary congestion and peripheral edema. Loop diuretics can be used to remove excess fluid accumulation in acute heart failure or can be used to relieve the congestive symptoms and prevent further fluid accumulation.
Chronic kidney disease CKD and acute kidney insult AKI are usually associated with volume overload because of the inability of the kidneys to excrete the salt and water. Nephrotic syndromes are associated with hypoalbuminemi a , which results in driving the water from vascular compartments into the interstitial space, therefore affected patients usually present with volume depletion.
Thus, diuretics should be used in nephrotic syndrome only in cases of severe edema or when there is no significant volume depletion. Liver cirrhosis releases vasodilators which stimulate the aldosterone release and salt and water retention and causes hypoalbuminemia.
Loop diuretics are commonly used in chronic liver patients with ascitis. Diuretics are commonly used in the treatment of hypertension by increasing water and sodium loss. They can be used as the first-line treatment or as an adjunctive treatment with other hypotensive regimens.
Loop diuretics increase the calcium excretion by the kidneys; therefore can be used in the treatment of hypercalcemia. Loop diuretic is usually combined with mannitol in the treatment of cerebral edema to decrease the intracranial pressure. It acts by inhibiting the local brain transport mechanisms, but not by its effect on salt and water excretion. Large doses of diuretics can lead to volume depletion, with the following subsequent consequences:. In the presence of the antidiuretic hormone ADH , the high osmotic pressure in the medullary interstitium allows NaCl reabsorption through collecting ducts via the osmotic gradient between the lumen and hypertonic interstitium, resulting in the formation of concentrated urine.
Loop diuretics inhibit this normal physiological process resulting in increased sodium and water excretion. Diuretic-induced volume depletion stimulates ADH secretion from the posterior pituitary, but its effect on the kidneys is limited because of the impairment of lumen-medullary osmotic gradient. Increased distal delivery of sodium to the collecting duct results in an increased tubular exchange of sodium for potassium with subsequently increased excretion of potassium resulting in hypokalemia.
Diuretic-induced volume depletion stimulates mineralocorticoids aldosterone release from the adrenal gland. Aldosterone increases the rate of potassium secretion by:.
Most of the reabsorbed potassium from the ascending limb of the loop of Henle via Na-K-2Cl cotransporters is recycled again back to the tubular lumen to drive further absorption of NaCl.
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