Review of Medical Physiology - William F. Ganong 2002

Urine Formation and Excretion
Renal Function and Urination
Diuretics

Chloride Excretion

Chloride reabsorption is enhanced when HCO₃ reabsorption decreases, and vice versa. Consequently, the plasma Cl concentration is inversely proportional to the HCO₃ concentration, thereby maintaining a constant anion balance. In certain situations, the movement of Cl can be explained by passive diffusion. However, In addition to this, Cl is also actively transported across the renal tubules.

Although a detailed review of diuretics is beyond our scope, examining their Mechanisms of action provides an excellent opportunity to review the factors influencing urine volume and electrolyte excretion. These mechanisms are summarized in Table 38-11. Water, alcohol, osmotic diuretics, xanthines, and acidifying salts have limited clinical value, while vasopressin antagonists are used solely for research purposes.

Class="center">Table 38-11. MECHANISM OF ACTION of Various Diuretics

Carbonic anhydrase inhibitors have only a moderate diuretic effect, but because they suppress acid secretion (by reducing carbonic acid generation), they exhibit a sustained action. As a result of decreased H⁺ secretion, not only is Na⁺ excretion enhanced, but HCO₃ reabsorption is also inhibited. Since H⁺ and K⁺ ions compete with each other and with Na⁺, the reduction in H⁺ secretion facilitates K⁺ secretion and excretion.

Another factor determining The rate of K⁺ secretion is The amount of Na⁺ delivered to the Na⁺-K⁺ exchange site in the distal tubule. Thiazide diuretics, furosemide, ethacrynic acid, and bumetanide act proximally to this site; the increased delivery of Na⁺ enhances K⁺ secretion. Significant urinary K⁺ loss is an undesirable side effect of these diuretics. Thiazides inhibit the Na⁺-Cl^- cotransporter in the early segment of the distal tubule (Fig. 38-25). Furosemide, ethacrynic acid, and bumetanide inhibit Na⁺ and Cl reabsorption in the thick ascending limb of the loop of Henle by blocking the Na⁺-K⁺-2Cl^- cotransporter (see Fig. 38-16). Spironolactone, triamterene, and amiloride act directly on the Na⁺-K⁺ exchange mechanism, causing K⁺ retention and, in some cases, mild hyperkalemia.