Osmotic diuretics owe their effects to the physical retention of fluid within the nephron rather than to direct action on cellular sodium transport. These compounds are not electrolytes, and they are freely filtered at the glomerulus and not reabsorbed to a significant extent. Ideally, these drugs should be water-soluble compounds, well absorbed after oral administration, freely filtered at the glomerulus, poorly reabsorbed by the tubule, and devoid of pharmacological effects. The prototype is mannitol (Osmitroî), an unmetabolizable poly-saccharide derivative of sucrose. Other clinically available osmotic diuretics include glycerin (Glycerol, Osmoglyn, and the topical agent Ophthalgan), isosorbide (Ismotic), and urea (Ureaphil, Urevert). Since these osmotic agents act in part to retard tubule fluid reabsorption, the amount of diuresis produced is proportional to the quantity of osmotic diuretic administered. Therefore, unless large quantities of a particular osmotic diuretic are given, the increase in urinary volume will not be marked.
Ideally, the distribution of osmotic diuretics should be largely confined to the vascular system, although this can lead to excessive expansion of the vascular compartment. Such an overexpansion could precipitate pulmonary edema or increase cardiac work or both. This is largely the result of rapid transfer of fluid from the interstitial to the vascular compartment. Practically speaking, however, few osmotic diuretics are available for therapeutic use. These agents, therefore, should be given cautiously to patients with compromised cardiac function.
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