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Absorption reabsorption

The magnitude and rates of zinc absorption, reabsorption and secretion. [Pg.70]

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]

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]

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]

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]

Diuretics promote the urinary excretion of sodium and water by inhibiting the absorption of filtered fluid across the renal tubular epithelium. The ensuing reduction in Na reabsorption reduces the Na content of the body, the critical determinant of extracellular and plasma fluid volumes. Thus, the use of diuretics is primarily indicated in the treatment of edematous diseases and of arterial hypertension. [Pg.429]

As in gastrointestinal absorption, the lipophillic nonionic form of a drug is more susceptible to reabsorption from the renal tubules by simple diffusion. Therefore,... [Pg.448]

Figure 5,4 Pharmacokinetics. The absorption distribution and fate of drugs in the body. Routes of administration are shown on the left, excretion in the urine and faeces on the right. Drugs taken orally are absorbed from the stomach and intestine and must first pass through the portal circulation and liver where they may be metabolised. In the plasma much drug is bound to protein and only that which is free can pass through the capillaries and into tissue and organs. To cross the blood brain barrier, however, drugs have to be in an unionised lipid-soluble (lipophilic) form. This is also essential for the absorption of drugs from the intestine and their reabsorption in the kidney tubule. See text for further details... Figure 5,4 Pharmacokinetics. The absorption distribution and fate of drugs in the body. Routes of administration are shown on the left, excretion in the urine and faeces on the right. Drugs taken orally are absorbed from the stomach and intestine and must first pass through the portal circulation and liver where they may be metabolised. In the plasma much drug is bound to protein and only that which is free can pass through the capillaries and into tissue and organs. To cross the blood brain barrier, however, drugs have to be in an unionised lipid-soluble (lipophilic) form. This is also essential for the absorption of drugs from the intestine and their reabsorption in the kidney tubule. See text for further details...
Prolonged administration of loop diuretics can lead to a second type of diuretic resistance. Enhanced delivery of sodium to the distal tubule can result in hypertrophy of distal convoluted cells.17 Subsequently, increased sodium chloride absorption occurs in the distal tubule which diminishes the effect of the loop diuretic on sodium excretion. Addition of a distal convoluted tubule diuretic, such as metolazone or hydrochlorothiazide, to a loop diuretic can result in a synergistic increase in urine output. There are no data to support the efficacy of one distal convoluted tubule diuretic over another. The common practice of administering the distal convoluted tubule diuretic 30 to 60 minutes prior to the loop diuretic has not been studied, although this practice may first inhibit sodium reabsorption at the distal convoluted tubule before it is inundated with sodium from the loop of Henle. [Pg.366]

The renal excretion of drugs depends on glomerular filtration, tubular secretion, and tubular absorption. A twofold increase in glomerular filtration occurs in the first 14 days of life [36], The glomerular filtration rate continues to increase rapidly in the neonatal period and reaches a rate of about 86 mL/min per 1.73 m2 by 3 months of age. Children 3-13 years of age have an average clearance of 134 mL/min per 1.73 m2 [37]. Tubular secretion approaches adult values between 2 and 6 months [11], There is more variability observed in maturation of tubular reabsorption capacity. This is likely linked to fluctuations in urinary pH in the neonatal period [38],... [Pg.668]

When D and A are similar molecules emission-reabsorption cannot be very important due to the usually small overlap of the emission and absorption spectra. Also, this mechanism should not be important for triplet-triplet energy transfer because of (a) low phosphorescence quantum yields in fluid solutions and (b) the low oscillator strengths for singlet-triplet absorption. [Pg.145]

Shu, C., et al. Mechanism of intestinal absorption and renal reabsorption of an orally active ace inhibitor uptake and transport of fosinopril in cell cultures. Drug Metab. Dispos. 2001, 29, 1307-1315. [Pg.272]

If the energy is transferred by trivial emission/reabsorption, it will lengthen the measured lifetime of the donor emission, not shorten it as happens in resonance energy transfer. This comes about because intervening absorption and emission processes take place prior to the final fluorescence emission (the reabsorption cannot take place until the photon has been emitted) the two processes do not compete dynamically, but follow in a serial fashion. In FRET, such an emission/reabsorption process does not occur, and the fluorescence lifetime of the donor decreases. This is an experimental check for reabsorption/reemission. [Pg.36]

The answer is e. (Katzung, p 254.) Furosemide affects the re absorption of uric acid in the proximal tubule. It increases uric acid reabsorption... [Pg.217]

Hydrochlorothiazide has its proposed site of action at the distal convoluted tubule or, more specifically, at the early portion of the distal tubule. Hydrochlorothiazide inhibits the reabsorption of Na and Cl. It also promotes the reabsorption of Ca back into the blood, but inhibits the re absorption of Mg from the renal tubular fluid. The K-sparing diuretic agents (spironolactone, triamterene, and amiloride) have their site of action in the nephron at the late distal tubule and the collecting duct. These diuretic agents only cause a mild natriuretic effect... [Pg.220]

The a ns wer is a. (Hardman, pp 1525-1528.) Pa r a thyroid ho r m o ne is synthesized by and released from the parathyroid gland increased synthesis of PTI1 is a response to low serum Ca concentrations. Resorption and mobilization of Ca and phosphate from bone are increased in response to elevated PTI1 concentrations. Replacement of body stores of Ca is enhanced by the capacity of PTH to promote increased absorption of Ca by the small intestine in concert with vitamin D, which is the primary factor that enhances intestinal Ca absorption. Parathyroid hormone also causes an increased renal tubular reabsorption of Ca and excretion of phosphate. As a consequence of these effects, the extracellular Ca concentration becomes elevated. [Pg.257]

High phosphate diets cause decreased Ca absorption, secondary hyperparathyroidism, accelerated bone resorption and soft tissue calcification in some animals, but not in normal humans. Although phosphates may decrease Ca absorption in man at very high (> 2000 mg/day) Ca intakes, they do not do so at more moderate Ca levels and enhance Ca absorption at very low levels (< 500 mg/day). Phosphates increase renal tubular reabsorption and net retention of Ca. At low Ca intakes, phosphates stimulate parathyroid hormone (PTH) secretion without causing net bone resorption. [Pg.33]

Figure 15.2 Transport proteins involved in the intestinal absorption and the renal and hepatic excretion of drugs. In the intestine, drugs are taken up from the luminal side into enterocytes before the subsequent elimination into blood. In hepatocytes, drugs are taken up from the blood over the basolateral membrane and excreted over the canalicular membrane into bile. In the renal epithelium, drugs undergo secretion (drugs are taken up from the blood and excreted into the urine) or reabsorption (drugs are taken up from the urine and are excreted back into blood). Uptake transporters belonging to the SLC transporter superfamily are shown in red and export pumps... Figure 15.2 Transport proteins involved in the intestinal absorption and the renal and hepatic excretion of drugs. In the intestine, drugs are taken up from the luminal side into enterocytes before the subsequent elimination into blood. In hepatocytes, drugs are taken up from the blood over the basolateral membrane and excreted over the canalicular membrane into bile. In the renal epithelium, drugs undergo secretion (drugs are taken up from the blood and excreted into the urine) or reabsorption (drugs are taken up from the urine and are excreted back into blood). Uptake transporters belonging to the SLC transporter superfamily are shown in red and export pumps...
Like most halogenated hydrocarbon pesticides, very little of the chlordecone or its metabolites is excreted via the urine. Because of the apparent enterohepatic recirculation of chlordecone and chlordecone alcohol, most experimental approaches to chlordecone detoxification have focused on limiting reabsorption from the gastrointestinal tract using cholestyramine (Boylan et al. 1978 Cohn et al. 1978), liquid paraffin (Richter et al. 1979), and chlorella and chlorella- derived sporopollenin (Pore 1984). No information was found that indicated that mirex undergoes enterohepatic recirculation, so it is not known whether use of these therapies would be effective in reducing absorption of mirex. [Pg.149]


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See also in sourсe #XX -- [ Pg.48 , Pg.54 ]




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Reabsorption

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