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Reabsorption, tubular

The process of tubular reabsorption is essential for the conservation of plasma constituents important to the body, in particular electrolytes and nutrient molecules. This process is highly selective in that waste products and substances with no physiological value are not reabsorbed, but instead excreted in the urine. Furthermore, reabsorption of many substances, such as Na+, H+, and Ca++ ions, and water is physiologically controlled. Consequently, volume, osmolarity, composition, and pH of the extracellular fluid are precisely regulated. [Pg.316]

Throughout its length, the tubule of the nephron is composed of a single layer of epithelial cells. Furthermore, the tubule is close to the peritubular capillaries, so reabsorption involves movement of a substance along the following pathway  [Pg.316]

Tubular reabsorption is considered passive when each of the steps in transepithelial transport takes place without the expenditure of energy. In other words, the movement of a given substance is from an area of high concentration to an area of low concentration by way of passive diffusion. Water is passively reabsorbed from the tubules back into the peritubular capillaries. [Pg.317]

Active reabsorption occurs when the movement of a given substance across the luminal surface or the basolateral surface of the tubular epithelial cell requires energy. Substances that are actively reabsorbed from the tubule include glucose amino acids and Na+, POy3, and Ca++ ions. Three generalizations can be made regarding the tubular reabsorption of sodium, chloride, and water  [Pg.317]

In other words, when sodium is reabsorbed, chloride and water follow it. [Pg.317]


As a general rule, increases of renal blood flow and/ or glomerular filtration rate (GFR) correlate rather well with increased urinary excretion of solutes and water. The underlying causes for this correlation are not fully understood, but they reflect incomplete adjustments of tubular reabsorption to an increase of tubular electrolyte load. [Pg.429]

Kir 1.1. Bartter Syndrome. Several mutations in the core region as well as in the N and C terminus of Kir 1.1 are found in patients with hyperprostaglandin E syndrome (HPS renal disorder resulting from impairment of tubular reabsorption), an antenatal form of Bartter syndrome. Some of these mutations result in the loss of function of Kiri. 1 channels causing impaired renal K+ secretion and NaCl reabsorption. [Pg.656]

Glycinuria results from a defect in renal tubular reabsorption. The defect in primary hyperoxaluria is the failure to catabolize glyoxylate formed by deamination of glycine. Subsequent oxidation of glyoxylate to oxalate results in urohthiasis, nephrocalcinosis, and early mortality from renal failure or hypertension. [Pg.250]

Possible causes of increased ratio of Cgm/Ccr pancreatitis can be liberation of a more readily excretable form of amylase, a protein with a molecular weight of 55,000 or less which can be easily filtered via the glomerulus and undergoes no appreciable tubular reabsorption. [Pg.212]

CF patients have larger volumes of distribution of many antibiotics due to an increased ratio of lean body mass to total body mass and lower fat stores. CF patients also have an enhanced total body clearance, although the exact mechanism has not been determined. Increased renal clearance, increased glomerular filtration rate, decreased protein binding, increased tubular secretion, decreased tubular reabsorption, extrarenal elimination, and increased metabolism have all been proposed as possible reasons for the increased clearance. [Pg.252]

Sodium bicarbonate increases renal tubular reabsorption of amphetamine, resulting in a prolonged amphetamine elimination half-life be aware of this combination. [Pg.533]

Probenecid is a uricosuric agent that blocks the tubular reabsorption of uric acid, increasing its excretion. Because of its mechanism of action, probenecid is contraindicated in patients with a history of uric acid stones or nephropathy. Probenecid loses its effectiveness as renal function declines and should be avoided when the creatinine clearance is 50 mL/minute or less. Its uricosuric effect is counteracted by low aspirin doses, which many patients receive for prophylaxis of coronary heart disease. [Pg.896]

The glomerular filtration rate (GFR) in normal males is estimated to be 125mL/min, and the results of the example calculation suggest that the drug is cleared by GFR. If the RCR had been less than 125 mL/min, tubular reabsorption of the drug would have been suspected. If it had been greater than 125 mL/min, tubular secretion would have been involved in the drug elimination. [Pg.85]

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]

Araki S, Aono H, Yokoyama K, et al. 1986. Filterable plasma concentration, glomerular fdtration, tubular reabsorption and renal clearance of heavy metals and organic substances in metal workers. Arch Environ Health 41 216-221. [Pg.487]

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]

The answer is a. (Hardman, pp 16-20.) Sodium bicarbonate is excreted principally in the urine and alkalinizes it. Increasing urinary pH interferes with the passive renal tubular reabsorption of organic acids (such as aspirin and phenobarbital) by increasing the ionic form of the drug in the tubular filtrate. This would increase their excretion. Excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be enhanced by acidifying the urine. [Pg.275]

Probenecid and sulfinpyrazone increase the renal clearance of uric acid by inhibiting the renal tubular reabsorption of uric acid. They should only be... [Pg.20]

Approximately 50% of the dose is excreted renally, and tubular reabsorption may be prominently involved. [Pg.610]

Decreases Ca transport into cells, interferes with Ca -Na active transport system, increases renal tubular reabsorption of Ca and increases serum Ca and parathyroid concentrations ... [Pg.780]

Hyperchloremic acidosis has been noted in some cases (B7, K13) this is presumably due to defective tubular reabsorption of bicarbonate. Phosphate-losing rickets or marked hypokalemia have not as yet been reported in galactosemia, but some cases show roentgenological evidence of osteoporosis (M2), and Holzel et al. (H8) record low levels of serum potassium. [Pg.21]

The urinary amino acids reflect both their high concentration in the blood, due to poor functioning of the liver, and failure of renal tubular reabsorption. The phenolic acids and tyrosine in the urine are evidence... [Pg.73]

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]

One of the unique advantages of renal cell culture rests in making possible the study of the directional aspects of drug exposure and cellular injury that operate in vivo. The technology to grow renal epithelial cells on filter inserts for this purpose has recently been made available (Figure 17.4). This potential provides the opportunity to study compounds that interact or accumulate within the renal tubular epithelium in vivo via tubular reabsorption from the luminal surface or extraction... [Pg.672]

Cojocel, C., Dociu, N., Maita, K., Sleight, S.D. and Hook, J.B. (1983). Effects of aminoglycosides on glomerular permeability, tubular reabsorption, and intracellular catabolism of the cationic low molecular weight protein lysozyme. Toxicol. Appl. Pharm. 39 129-139. [Pg.678]

Dietary salt restriction was one of the first successful therapeutic maneuvers for the reduction of blood pressure. During the past two decades, a variety of pharmacologic agents have been developed which promote diuresis by interfering with the tubular reabsorption of sodium. Although diuretic agents differ significantly in chemical structure and in their mechanism of action on the renal tubule, they all have in common the ability to decrease blood pressure. [Pg.82]

A plot of rate of transport against solute concentration in the tubule (Figure 8.3) shows fm, the tubular transport maximum to be analogous with Vmax for an enzyme, which is a maximum rate of solute transport across tubular cells. Assuming a fixed GFR, the point at which the plotted line begins to deviate from linearity, indicates that the substance exceeds a critical threshold concentration and begins to be excreted in the urine. When the plotted line reaches a plateau indicating that saturation point, that is tm has been reached, the rate of excretion is linear with increase in plasma concentration. The concept of fm as described here for tubular reabsorption applies equally well to carrier-mediated secretory processes. If the fm value for a particular is exceeded for any reason, there will be excretion of that solute in the urine. [Pg.265]

Reabsorbed This line also passes through the origin. It matches the filtered line until 11 mmol.l 1 and then starts to flatten out as it approaches maximal tubular reabsorption (TMax) Demonstrate that this value is 300 mg.min-1 on the y axis. [Pg.181]


See other pages where Reabsorption, tubular is mentioned: [Pg.381]    [Pg.270]    [Pg.466]    [Pg.211]    [Pg.138]    [Pg.303]    [Pg.97]    [Pg.803]    [Pg.362]    [Pg.1293]    [Pg.107]    [Pg.258]    [Pg.323]    [Pg.316]    [Pg.317]    [Pg.318]    [Pg.221]    [Pg.20]    [Pg.74]    [Pg.205]    [Pg.36]    [Pg.40]    [Pg.126]    [Pg.271]   
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See also in sourсe #XX -- [ Pg.33 ]

See also in sourсe #XX -- [ Pg.646 ]

See also in sourсe #XX -- [ Pg.25 ]

See also in sourсe #XX -- [ Pg.508 ]

See also in sourсe #XX -- [ Pg.646 ]

See also in sourсe #XX -- [ Pg.16 , Pg.125 ]




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