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Reabsorption

Spironolactone is the most clinically usehil steroidal aldosterone antagonist, and unlike GR antagonists, this compound is utilized much more frequendy than aldosterone agonists. Interfering with reabsorption and secretion in the late distal segment, this compound is predominantiy used with other diuretics. Canrenone, an olefinic metaboHte of spironolactone, and potassium canrenoate, in which the C-17 lactone has been hydrolyzed open, are also potent mineralocorticoid antagonists. [Pg.109]

Only a small (ca 3%) fraction of ingested or inhaled manganese is absorbed, which occurs primarily by the intestines (209). Once absorbed, manganese is regulated by the Hver, where it is excreted into the bile and passes back into the intestine, where some reabsorption may occur (210). Manganese is elirninated almost exclusively (>95%) by the bile in the gastrointestinal tract. [Pg.526]

Factors controlling calcium homeostasis are calcitonin, parathyroid hormone(PTH), and a vitamin D metabolite. Calcitonin, a polypeptide of 32 amino acid residues, mol wt - SGOO, is synthesized by the thyroid gland. Release is stimulated by small increases in blood Ca " concentration. The sites of action of calcitonin are the bones and kidneys. Calcitonin increases bone calcification, thereby inhibiting resorption. In the kidney, it inhibits Ca " reabsorption and increases Ca " excretion in urine. Calcitonin operates via a cyclic adenosine monophosphate (cAMP) mechanism. [Pg.376]

Parathyroid hormone, a polypeptide of 83 amino acid residues, mol wt 9500, is produced by the parathyroid glands. Release of PTH is activated by a decrease of blood Ca " to below normal levels. PTH increases blood Ca " concentration by increasing resorption of bone, renal reabsorption of calcium, and absorption of calcium from the intestine. A cAMP mechanism is also involved in the action of PTH. Parathyroid hormone induces formation of 1-hydroxylase in the kidney, requited in formation of the active metabolite of vitamin D (see Vitamins, vitamin d). [Pg.376]

Ozone can be analyzed by titrimetry, direct and colorimetric spectrometry, amperometry, oxidation—reduction potential (ORP), chemiluminescence, calorimetry, thermal conductivity, and isothermal pressure change on decomposition. The last three methods ate not frequently employed. Proper measurement of ozone in water requites an awareness of its reactivity, instabiUty, volatility, and the potential effect of interfering substances. To eliminate interferences, ozone sometimes is sparged out of solution by using an inert gas for analysis in the gas phase or on reabsorption in a clean solution. Historically, the most common analytical procedure has been the iodometric method in which gaseous ozone is absorbed by aqueous KI. [Pg.503]

The process of reabsorption depends on the HpophiHc—hydrophiHc balance of the molecule. Charged and ioni2ed molecules are reabsorbed slowly or not at all. Reabsorption of acidic and basic metaboHtes is pH-dependent, an important property in detoxification processes in dmg poisoning. Both passive and active carrier-mediated mechanisms contribute to tubular dmg reabsorption. The process of active tubular secretion handles a number of organic anions and cations, including uric acid, histamine, and choline. Dmg metaboHtes such as glucuronides and organic acids such as penicillin are handled by this process. [Pg.270]

In subsequent studies attempting to find a correlation of physicochemical properties and antimicrobial activity, other parameters have been employed, such as Hammett O values, electronic distribution calculated by molecular orbital methods, spectral characteristics, and hydrophobicity constants. No new insight on the role of physiochemical properties of the sulfonamides has resulted. Acid dissociation appears to play a predominant role, since it affects aqueous solubiUty, partition coefficient and transport across membranes, protein binding, tubular secretion, and reabsorption in the kidneys. An exhaustive discussion of these studies has been provided (10). [Pg.467]

Hydroxy vitamin D pools ia the blood and is transported on DBF to the kidney, where further hydroxylation takes place at C-1 or C-24 ia response to calcium levels. l-Hydroxylation occurs primarily ia the kidney mitochondria and is cataly2ed by a mixed-function monooxygenase with a specific cytochrome P-450 (52,179,180). 1 a- and 24-Hydroxylation of 25-hydroxycholecalciferol has also been shown to take place ia the placenta of pregnant mammals and ia bone cells, as well as ia the epidermis. Low phosphate levels also stimulate 1,25-dihydtoxycholecalciferol production, which ia turn stimulates intestinal calcium as well as phosphoms absorption. It also mobilizes these minerals from bone and decreases their kidney excretion. Together with PTH, calcitriol also stimulates renal reabsorption of the calcium and phosphoms by the proximal tubules (51,141,181—183). [Pg.136]

Three hormones regulate turnover of calcium in the body (22). 1,25-Dihydroxycholecalciferol is a steroid derivative made by the combined action of the skin, Hver, and kidneys, or furnished by dietary factors with vitamin D activity. The apparent action of this compound is to promote the transcription of genes for proteins that faciUtate transport of calcium and phosphate ions through the plasma membrane. Parathormone (PTH) is a polypeptide hormone secreted by the parathyroid gland, in response to a fall in extracellular Ca(Il). It acts on bones and kidneys in concert with 1,25-dihydroxycholecalciferol to stimulate resorption of bone and reabsorption of calcium from the glomerular filtrate. Calcitonin, the third hormone, is a polypeptide secreted by the thyroid gland in response to a rise in blood Ca(Il) concentration. Its production leads to an increase in bone deposition, increased loss of calcium and phosphate in the urine, and inhibition of the synthesis of 1,25-dihydroxycholecalciferol. [Pg.409]

Fiber components are the principal energy source for colonic bacteria with a further contribution from digestive tract mucosal polysaccharides. Rate of fermentation varies with the chemical nature of the fiber components. Short-chain fatty acids generated by bacterial action are partiaUy absorbed through the colon waU and provide a supplementary energy source to the host. Therefore, dietary fiber is partiaUy caloric. The short-chain fatty acids also promote reabsorption of sodium and water from the colon and stimulate colonic blood flow and pancreatic secretions. Butyrate has added health benefits. Butyric acid is the preferred energy source for the colonocytes and has been shown to promote normal colonic epitheUal ceU differentiation. Butyric acid may inhibit colonic polyps and tumors. The relationships of intestinal microflora to health and disease have been reviewed (10). [Pg.70]

In normal human subjects, ANP infusion for one hour causes increased absolute and fractional sodium excretion, urine flow, GFR, and water clearance (53—55). As shown in many in vitro and in vivo animal studies, ANP achieves this by direct effect on the sodium reabsorption in the inner medullary collecting duct, ie, by reducing vasopressin-dependent free-water and sodium reabsorption leading to diuresis and by indirect effect through increased hemodynamic force upon the kidney. ANP inhibits the release of renin and aldosterone resulting in the decreased plasma renin activity and aldosterone concentration (56,57). [Pg.208]

Vitamin D is a family of closely related molecules that prevent rickets, a childhood disease characterized by inadequate intestinal absorption and kidney reabsorption of calcium and phosphate. These inadequacies eventually lead to the demineralization of bones. The symptoms of rickets include bowlegs,... [Pg.605]

Resorbierung, /. resorption, reabsorption. Resorcin, n. resorcinol, resorcin, -blau, n, resorcin blue, -gelb, n. resorcin yellow. Resorzin, n. resorcinol, resorcin, reap., abbrev. of respektive. respektive, adv. respectively, or rather, or. Respirationsnahrungsnuttel, n. respiratory food. [Pg.364]

In the kidney, ANG II reduces renal blood flow and constricts preferentially the efferent arteriole of the glomerulus with the result of increased glomerular filtration pressure. ANG II further enhances renal sodium and water reabsorption at the proximal tubulus. ACE inhibitors thus increase renal blood flow and decrease sodium and water retention. Furthermore, ACE inhibitors are nephroprotective, delaying the progression of glomerulosclerosis. This also appears to be a result of reduced ANG II levels and is at least partially independent from pressure reduction. On the other hand, ACE inhibitors decrease glomerular filtration pressure due to the lack of ANG II-mediated constriction of the efferent arterioles. Thus, one important undesired effect of ACE inhibitors is impaired glomerular filtration rate and impaired kidney function. [Pg.9]

Airway surface liquid (ASL) is the very thin fluid layer (<7 (llM) maintained at the apical membrane of airway epithelia. ASL thickness is maintained by a tight control of fluid reabsorption and/or secretion, mediated by sodium and/or chloride channels. [Pg.51]

Anion exchange resins are basic polymers with a high affinity for anions. Because different anions compete for binding to them, they can be used to sequester anions. Clinically used anion exchange resins such as cholestyramine are used to sequester bile acids in the intestine, thereby preventing their reabsorption. As a consequence, the absorption of exogenous cholesterol is decreased. The accompanying increase in low density lipoprotein (LDL)-receptors leads to the removal of LDL from the blood and, thereby, to a reduction of LDL cholesterol. This effect underlies the use of cholestyramine in the treatment of hyperlipidaemia. [Pg.90]

Anti-gout Drugs. Figure 2 Reabsorption and secretion of uric acid in the proximal renal tubulus. (a) Normal situation. Uric acid is completely reabsorbed in the proximal segment of the renal tubulus and secreted more distally. (b) Situation in untreated hyperuricemia. [Pg.136]


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Absorption reabsorption

Antidiuretic hormone water reabsorption controlled

Ascorbic acid tubular reabsorption

Bicarbonate reabsorption

Bicarbonate renal tubular reabsorption

Bile acid reabsorption

Bile salts reabsorption

Calcium reabsorption, renal, mechanism

Calcium renal reabsorption

Calcium renal tubular reabsorption

Calcium, absorption reabsorption renal

Cephalosporin tubular reabsorption

Chloride reabsorption

Chloride, renal tubular reabsorption

Creatinine proximal tubule reabsorption

Cross-section for resonant reabsorption

Diamond reabsorption

Distal tubule water reabsorption

Drug elimination tubular reabsorption

Excretion and reabsorption of drugs

Excretion tubular reabsorption

Excretion tubular reabsorption, passive

Filtration and reabsorption

Fluorescence reabsorption

Function reabsorption

Glucose Reabsorption

Glucose proximal tubule reabsorption

Glucuronide tubular reabsorption

Hemoglobin Reabsorption

Henle, loop potassium reabsorption

Kidney Glucose reabsorption

Kidney Sodium reabsorption

Kidney Uric acid reabsorption

Kidney calcium reabsorption

Kidney drug reabsorption

Kidney tubular reabsorption

Kidneys chloride reabsorption

Kidneys reabsorption

Kidneys reabsorption from

Magnesium reabsorption

Magnesium renal tubular reabsorption

Maximum tubular reabsorptive capacity

NaCI Reabsorption in the Kidney

NaCl reabsorption, kidney

Passive reabsorption

Potassium reabsorption

Potassium renal tubular reabsorption

Presecretory reabsorption

Presecretory reabsorption defect

Prostaglandin reabsorption

Proximal tubule potassium reabsorption

Proximal tubule reabsorption

Proximal tubule, albumin reabsorption

Pyrazinamide tubular reabsorption

Reabsorption Lines of Oxygen and Water

Reabsorption and Reemission

Reabsorption of free radicals

Reabsorption of uric acid

Reabsorption sodium

Reabsorption water

Reabsorption, catalyzed

Reabsorption, drugs

Reabsorption, passive renal

Reabsorption, renal tubular

Renal disease reabsorption mechanisms

Renal reabsorption system

Renal tubular reabsorption defects

Salt reabsorption

Sodium bicarbonate renal tubular reabsorption

Sodium chloride reabsorption

Sodium chloride reabsorption, kidney

Sodium reabsorption Aldosterone

Sodium, renal tubular reabsorption

Stimulation of Renal Calcium Reabsorption

Subretinal fluid reabsorption

Tubular reabsorption

Tubular reabsorption deficiency

Tubular reabsorption renal handling

Tubules reabsorption

Urate reabsorption

Uric Reabsorption

Uric acid proximal tubule reabsorption

Uric acid reabsorption

Vitamin D (cont calcium reabsorption

Vitamin renal reabsorption

Water renal tubular reabsorption

Zircon reabsorption lines

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