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Water renal tubular reabsorption

Elevates osmotic pressure of glomerular filtrate, increases flow of water into interstitial fluid and plasma, inhibiting renal tubular reabsorption of sodium, chloride, producing diuresis. Enhances flow of water from eye into plasma, reducing intraocular pressure (IOP)... [Pg.348]

The low plasma PCO2 leads to decreased renal tubular reabsorption of bicarbonate and increased renal excretion ofNa , K, and water. Water also is lost by salicylate-induced sweating (especially in the presence of hyperthermia) and hyperventilation dehydration, which can be profound, particularly in children, rapidly occurs. Because more water than electrolyte is lost through the lungs and by sweating, the dehydration is associated with hypernatremia. Prolonged exposure to high doses of salicylate also causes depletion ofK due to both renal and extrarenal factors. [Pg.444]

Probenecid inhibits renal tubular reabsorption of water and by this meehanism enhanees the urinary excretion of uric acid. This lowers the level of urate in the serum. It thus serves as a potent uricosuric agent in the treatment of gout. Probenecid also blocks the renal tubular seeretion of penicillins and cephalosporins. It is, therefore, used as an adjuvant therapy with penicillin V or G, ampicillin, cloxacillin, oxacillin, methicillin and naficillin to increase and prolong their plasma levels. Besides it also enhances the plasma levels of anti-inflammatory agents like naproxen and indomethacin, and a host of medicinal compounds such as sulphonamides, sulphonylureas, dapsone, etc. [Pg.539]

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 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]

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. [Pg.519]

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. [Pg.414]

Kidney Methylxanthines exert mild diuretic action by inhibiting tubular reabsorption of sodium and water. In addition, it increases renal blood flow and glomerular filtration rate. [Pg.233]

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. [Pg.320]

Many diuretic agents (loop diuretics, thiazides, amiloride, and triamterene) 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 (spironolactone). [Pg.347]

Elhawary AM, Pang CC, b I-Adrenergic receptors mediate renal tubular sodium and water reabsorption in the rat. Br J... [Pg.461]

The volume of urine is determined both by the fall in glomerular filtration rate and by the reduced tubular reabsorption of water. The balance determines whether renal failure, if it occurs, is oliguric or nonoliguric. Retention of sodium and water help to conserve body water and... [Pg.4]

Cyclophosphamide can also cause tubular necrosis in experimental animals [82]. No clinical counterpart has been described, despite careful assessment in patients receiving high doses of cyclophosphamide [83, 84]. Although detectable alterations of renal function tests are absent, subtle changes in renal tubular physiology have been noted. Bode et al. [85] studied the mechanism of water retention that occurs following cyclophosphamide. They concluded that cyclophosphamide directly affected the tubules, causing increased water reabsorption and sodium loss. This water retention is self-hmited to a day or two and does not present a major dinical problem. [Pg.359]

Salt and water retention result from increased proximal tubular reabsorption due to reduced renal perfusion pressure and reflex stimulation of renal tubular a adrenergic receptors. Similar antinatriuretic effects are observed with other arteriolar dilators (e.g., diazoxide and hydralazine). [Pg.557]

Most sodium and water reabsorption occurs throughout the renal tubular segments. Diuretics affect one or more of these segments. Every one and one-half hours the kidneys (glomeruli) clean the body s extracellular fluid (ECF). [Pg.384]


See other pages where Water renal tubular reabsorption is mentioned: [Pg.148]    [Pg.382]    [Pg.345]    [Pg.548]    [Pg.52]    [Pg.76]    [Pg.9]    [Pg.57]    [Pg.491]    [Pg.709]    [Pg.562]    [Pg.97]    [Pg.101]    [Pg.286]    [Pg.301]    [Pg.26]    [Pg.116]    [Pg.1679]    [Pg.117]    [Pg.93]    [Pg.113]    [Pg.248]    [Pg.646]    [Pg.259]    [Pg.108]    [Pg.462]    [Pg.91]    [Pg.182]    [Pg.184]    [Pg.484]    [Pg.646]    [Pg.7]    [Pg.91]    [Pg.3668]   
See also in sourсe #XX -- [ Pg.146 , Pg.147 ]




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