Diuretics An Overview

Diuretics (saluretics) elicit increased production of urine (diuresis). In the strict sense, the term is applied to drugs with a direct renal action. The predominant action of such agents is to augment urine excretion by inhibiting the reabsorption of NaCl and water.

The most important indications for diuretics are:

Mobilization of edemas (A): In edema there is swelling of tissues due to accumulation of fluid, chiefly in the extracellular (interstitial) space. When a diuretic is given, increased renal excretion of Na+ and H2O causes a reduction in plasma volume with hemoconcentra-tion. As a result, plasma protein concentration rises along with oncotic pressure. As the latter operates to attract water, fluid will shift from interstitium into the capillary bed. The fluid content of tissues thus falls and the edemas recede. The decrease in plasma volume and interstitial volume means a diminution of the extracellular fluid volume (EFV). Depending on the condition, use is made of: thiazides, loop diuretics, al-dosterone antagonists, and osmotic diuretics.

Antihypertensive therapy. Diuretics have long been used as drugs of first choice for lowering elevated blood pressure (p. 312). Even at low dosage, they decrease peripheral resistance (without significantly reducing EFV) and thereby normalize blood pressure.

Therapy of congestive heart failure. By lowering peripheral resistance, diuretics aid the heart in ejecting blood (reduction in afterload, pp. 132, 306); cardiac output and exercise tolerance are increased. Due to the increased excretion of fluid, EFV and venous return decrease (reduction in preload, p. 306). Symptoms of venous congestion, such as ankle edema and hepatic enlargement, subside. The drugs principally used are thiazides (possibly combined with K+-sparing diuretics) and loop diuretics.

Prophylaxis of renal failure. In circulatory failure (shock), e.g., secondary to massive hemorrhage, renal production of urine may cease (anuria). By means of diuretics an attempt is made to maintain urinary flow. Use of either osmotic or loop diuretics is indicated.

Massive use of diuretics entails a hazard of adverse effects (A): (1) the decrease in blood volume can lead to hypotension and collapse; (2) blood viscosity rises due to the increase in eryth-ro- and thrombocyte concentration, bringing an increased risk of intravascular coagulation or thrombosis.

When depletion of NaCl and water (EFV reduction) occurs as a result of diuretic therapy, the body can initiate counter-regulatory responses (B), namely, activation of the renin-angio-tensin-aldosterone system (p. 124). Because of the diminished blood volume, renal blood flow is jeopardized. This leads to release from the kidneys of the hormone, renin, which enzymatically catalyzes the formation of angiotensin I. Angiotensin I is converted to angioten-sin II by the action of angiotensin-con-verting enzyme (ACE). Angiotensin II stimulates release of aldosterone. The mineralocorticoid promotes renal reabsorption of NaCl and water and thus counteracts the effect of diuretics. ACE inhibitors (p. 124) augment the effectiveness of diuretics by preventing this counter-regulatory response.

Adverse Effects Diuretics
A. Mechanism of edema fluid mobilization by diuretics
Osmotic Diuretics
Blood Pressure Health

Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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