Kidneys chloride reabsorption

Although one thiazide diuretic may be 100 times more potent than another weight for weight, all these drugs have essentially the same properties. Their mechanism of action (inhibition of sodium and chloride reabsorption in the distal convoluted tubule of the kidney) is identical and they can therefore be dealt with as a group. Thiazidelike diuretics, structurally different from the thiazides, have similar actions. Thiazide and thiazide-like diuretics are listed in Table 1. 

In kidney, calcitonin increases the secretion of calcium, phosphate, and sodium. The natriuretic effect of calcitonin is associated with water loss, increased urine volume, and weight loss. The effect of calcitonin on sodium excretion is different from that of parathormone. While parathormone appears to favor a sodium for hydrogen exchange, which takes place in the distal tubules, calcitonin acts on the proximal tubule by blocking sodium and chloride reabsorption [37]. 

The nephronic parts of the kidney are the principal diuretic active sites for secreting ede-matic fluid from the organism. Diuretics basically increase secretion of water and salts from the kidneys by suppressing reabsorption of a few main ions (primarily sodium and chloride ions) however, secretion of calcium, potassium, magnesium, and hydrocarbonate ions also increases to some degree. 

Acetazolamide is an aromatic sulfonamide used as a carbonic anhydrase inhibitor. It facilitates production of alkahne urine with an elevated biocarbonate, sodium, and potassium ion concentrations. By inhibiting carbonic anhydrase, the drug suppresses reabsorption of sodium ions in exchange for hydrogen ions, increases reflux of bicarbonate and sodium ions and reduces reflux of chloride ions. During this process, chloride ions are kept in the kidneys to cover of insufficiency of bicarbonate ions, and for keeping an ion balance. Electrolytic contents of fluid secreted by the kidneys in patients taking carbonic anhydrase inhibitors are characterized by elevated levels of sodium, potassium, and bicarbonate ions and a moderate increase in water level. Urine becomes basic, and the concentration of bicarbonate in the plasma is reduced. 

Certain foreign compounds may cause the retention or excretion of water. Some compounds, such as the drug furosemide, are used therapeutically as diuretics. Other compounds causing diuresis are ethanol, caffeine, and certain mercury compounds such as mersalyl. Diuresis can be the result of a direct effect on the kidney, as with mercury compounds, which inhibit the reabsorption of chloride, whereas other diuretics such as ethanol influence the production of antidiuretic hormone by the pituitary. Changes in electrolyte balance may occur as a result of excessive excretion of an anion or cation. For example, salicylate-induced alkalosis leads to excretion of Na+, and ethylene glycol causes the depletion of calcium, excreted as calcium oxalate. 

They act on the kidney by depressing the mechanisms that govern the active reabsorption of sodium and chloride ions. They are rapidly excreted by the kidney but their use is hazardous because their action is believed to be due to inorganic mercury ions released by rupture of the carbon-to-mercury bond, probably followed by the firm attachment of the mercury ion to a sulphydryl group of a renal enzyme. The administration of dimercaprol (SO), a strong chelating agent for mercury, removes mercury from the kidney and terminates the diuretic action. It is of interest that Paracelsus used calomel (mercurous chloride) as a diuretic. 

NaPi-1 (SLC17A1), alternatively referred to as NPT1, was originally cloned as a transporter involved in the reabsorption of phosphate in the body. Expression of NaPi-1 in X. laevis oocytes induced saturable uptake of benzylpenicillin (189). This uptake does not depend on Na+ and H+, but on Cl- (190), and increasing extracellular concentration of chloride reduced the uptake of benzyl-penicillin (190). The substrates include faropenem, foscamet, and mevalonate, as well as benzylpenicillin (190). In contrast to the kidney, the expression is localized to the sinusoidal membrane of the liver (190). When the direction of the concentration gradient of Cl- is taken into consideration, the transport direction mediated by NaPi-1 is efflux from inside the cells to the blood and urine in the liver and kidney, respectively. 

The effect of urinary pH on drug ionization also has toxicological implications. For example, in cases of phenobarbital (a weak acid barbiturate) overdose the urine can be alkalinized (the pH elevated) by administering sodium bicarbonate to the patient. The resultant increase in pH shifts the dissociation equilibrium for this weak acid to the right, producing an increase in the proportion of the ionized form, less reabsorption in the kidneys, and more rapid elimination. Conversely, acidifying the urine with ammonium chloride will increase the excretion rate of drugs that are weak bases since they will be more protonated (ionized) and less reabsorbed (more polar, less lipophilic). 

Oxalate is excreted primarily by the kidney. Oxalate is freely filtered at the glomerulus, where its concentration is normally 1 5 pM. One of the few physiologic functions of oxalate occurs in the proximal tubule where it plays a role in transcellular reabsorption of chloride (mainly present as sodium chloride). Cl entry across the apical membrane is mediated by Cl /oxalate exchange (oxalate is recycled from the tubular lumen to the cell by oxalate/ sulfate exchange, in parallel with Na /sulfate cotransport) [4]. Early studies of renal oxalate clearance using radio-labeled oxalate showed secretion in almost all subjects studied. More recent studies using direct measurement of serum and urine... 

The proximal tubule is the most metabolically active part of the nephron, facilitating the reabsorption of 60% to 80% of the glomerular filtrate volume—including 70% of the filtered load of sodium and chloride, most of the potassium, glucose, bicarbonate, phosphate, and sulfate—and secreting 90% of the hydrogen ion excreted by the kidney (Table 45-1). 

Some of the rare causes of metabolic alkalosis due to potassium depletion are those found in subjects with either Cushing s syndrome, primary aldosteronism, or Bartter s syndrome. In Cushing s syndrome, the potassium ions and alkalosis are related to increased mineralocorticoid activity resulting from an increase in adrenocorticotropic hormone (ACTH), cortisol, deoxycorticosterone, and corticosterone. In primary aldosteronism, the effects of increased aldosterone are manifest on the distal tubule of the kidney. In Bartter s syndrome, the basic abnormality appears to be a defect in the reabsorption of chloride in the ascending limb of loop of Henle, leading to loss of potassium (12). 

Thiazide diuretics work by inhibiting sodium and chloride ion transport in the distal convoluted tubule of the kidney and therefore limit water reabsorption. Thiazides are particularly recommended in older people. A commonly used example of this type of diuretic is bendroflumethiazide. 

ADH is secreted in response to an increase in plasma sodium chloride concentration or a decrease in circulating blood volume. ADH acts on kidney collecting duct cells to increase water reabsorption. In this way plasma sodium chloride concentration and/or blood volume are restored to normal. ADH also acts as a vasoconstrictor, which helps to maintain blood pressure if circulating blood volume has fallen. 

Mineralocorticoids regulate ion balance by promoting reabsorption of sodium, chloride, and bicarbonate in the kidney. 

Contrary to PTH, calcitonin has a lowering action on blood Ca activity. It is synthesized in the parafollicular cells (C cells) in the thyroid. An increased blood Ca activity leads to calcitonin secretion, and within a few minutes both calcium and phosphate concentrations in plasma are lowered. This effect is accomplished by an effect on the bone cells, where calcium is bound as hydroxyapatite. Besides this effect, calcitonin also decreases intestinal uptake and renal reabsorption. Calcitonin inhibits the osteoclasts ( bone eater cells ) and hence reduces the amount of calcium and phosphate released from bone to the extracellular fluid. The effect on the kidneys leads to an increased excretion of calcium, phosphate, sodium, chloride, and water. 

The most important hormone secreted by the adrenal glands for salt balance is aldosterone. In the absence of this hormone, large quantities of sodium are excreted by the kidney and survival is only possible if a 0.9% NaCl solution is available in place of drinking water. Aldosterone, a steroid hormone acts on the kidney to cause sodium resorption in the distal convoluted tubule, partly in exchange for potassium. Increased sodium reabsorption raises the solute concentration of body fluids. Adrenal hormones in mammals also facilitate the resorption of sodium and chloride from sweat and saliva and also cause increased sodium resorption in the gut. Low sodium ion concentration triggers the secretion of aldosterone. But other body conditions like increased potassium concentration, decreased cardiac output and stress too can induce aldosterone secretion. 

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