Renal tubular reabsorption

Less is known of the impact of sex on tubular secretion or tubular reabsorption. Renal tubular secretion or... 

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. 

Vasopressin (Rtressin Synthetic) and its derivatives, namely lypressin (Diapid) and desmopressin (DDAVP), regulate the reabsorption of water by the kidneys. Vasopressin is secreted by the pituitary when body fluids must be conserved. An example of this mechanism may be seen when an individual has severe vomiting and diarrhea with little or no fluid intake. When this and similar conditions are present, die posterior pituitary releases the hormone vasopressin, water in die kidneys is reabsorbed into die blood (ie, conserved), and die urine becomes concentrated. Vasopressin exhibits its greatest activity on die renal tubular epithelium, where it promotes water resoqition and smooth muscle contraction throughout die vascular bed. Vasopressin has some vasopressor activity. 

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. 

Hesse, I.F.A. and Johns, E.J. (1984). The subtype of a-adrcnoceptor involved in the neural control of renal tubular sodium reabsorption in the rabbit. J. Physiol. 328, 527-538. 

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

The answers are 370-c, 371-d, 372-c. (Hardman, pp 697, 701, 705.) The loop diuretic ethacrynic acid has its site of action in the ascending limb of the loop of Henle. This drug inhibits the reabsorption of Na and Cl" by interfering with the Na+, K+, 2CL co-transport system. In addition, loop diuretics block the reabsorption of Mg and Ca from the renal tubular fluid into the blood in this segment of the nephron unit. 

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... 

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. 

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. 

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

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 ... 

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... 

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. 

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... 

The rate of total body clearance accounted for by the kidney. Its magnitude is determined by the net effects of glomerular filtration, tubular secretion and reabsorption, renal blood flow, and protein binding. 

Pharmacology A uricosuric and renal tubular blocking agent, probenecid inhibits the tubular reabsorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum uric acid levels. 

Pregabalin is eliminated from the systemic circulation primarily by renal excretion as unchanged drug, with a mean elimination half-life of 6.3 hours in subjects with normal renal function. Mean renal clearance was estimated to be 67 to 80.9 mL/min in young healthy subjects. Because pregabalin is not bound to plasma proteins, this clearance rate indicates that renal tubular reabsorption is involved. Pregabalin elimination is nearly proportional to Ccr. 

An additional contributing factor to the diuresis induced by osmotic diuretics is the increase in renal medullary blood flow that follows their administration. This medullary hyperemia reduces the cortex-meduUary osmolar gradient by carrying away interstitial Na+ and urea. This partial reduction of the osmolar gradient impairs normal reabsorption of tubular water, which occurs from the descending limb of Henle and the collecting duct. 

Ethanol is a diuretic. This effect may be caused by its ability to inhibit secretion of antidiuretic hormone from the posterior pituitary, which leads to a reduction in renal tubular water reabsorption. The large amount of fluid normally consumed with ethanol also contributes to increased urine production. 

Mechanism of Action An antigout agent that competitively inhibits reabsorption of uric acid at the proximal convoluted tubule. Also, inhibits renal tubular secretion of weak organic acids, such as penicillins. Therapeutic Effect Promotes uric acid excretion, reduces serum uric acid level, and increases plasma levels of penicillins and cephalosporins. 

While theoretically it is possible that botanicals with diuretic effects can increase drug excretion, most botanical diuretics are not as potent as furo-semide and are unlikely to result in significant interactions. Most botanicals also do not affect urinary pH significantly, and hence are unlikely to affect renal tubular reabsorption of drugs. Nevertheless, lithium toxicity was thought to be related to the use of a botanical diuretic mixture in a patient. If the toxicity indeed is related to the use of the botanical diuretic, the mechanism of action or the responsible constituent(s) is not known (48). 

This chapter is divided into three sections. The first section covers renal tubule transport mechanisms. The nephron is divided structurally and functionally into several segments (Figure 15-1, Table 15-1). Many diuretics exert their effects on specific membrane transport proteins in renal tubular epithelial cells. Other diuretics exert osmotic effects that prevent water reabsorption (mannitol), inhibit enzymes (acetazolamide), or interfere with hormone receptors in renal epithelial cells (aldosterone receptor blockers). The physiology of each segment is closely linked to the basic pharmacology of the drugs acting there, which is discussed in the second section. Finally, the clinical applications of diuretics are discussed in the third section. 

Renal function is depressed by opioids. It is believed that in humans this is chiefly due to decreased renal plasma flow. In addition, opioids have been found to have an antidiuretic effect in humans. Mechanisms may involve both the CNS and peripheral sites. Opioids also enhance renal tubular sodium reabsorption. The role of opioid-induced changes in antidiuretic hormone (ADH) release is controversial. Ureteral and bladder tone are increased by therapeutic doses of the opioid analgesics. Increased sphincter tone may precipitate urinary retention, especially in postoperative patients. Occasionally, ureteral colic caused by a renal calculus is made worse by opioid-induced increase in ureteral tone. 

Amino acids are precious components of the human organism and therefore urinary losses are small due to an efficient renal tubular reabsorption system. Because of this, and because the analytical approach is aimed at detecting catabolic... 

Reference values for amino acids in the urine show a rather sharp decrease from the neonatal period to adulthood (Table 2.1.6). This is mainly due to the maturation of the renal tubular reabsorption system, but is also the result of increasing muscle mass with age, giving rise to increasing creatinine production. 

In six healthy subjects, ampicillin caused an increase in urinary uric acid excretion this effect was attributed to competition for active renal tubular reabsorption of urate (SEDA-13, 212). 

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