Classification of diuretics

According to site of action and mechanism of action

  1. Acting at proximal convoluted tubules
  2. Osmotic diuretics

These drugs are  mannitole and urea

  1. Carbonic anhydrase inhibitors

These drugs are  Acetazolamide, methazolamide

  1. Acidifying drugs

These agents are  ammonium chloride

iv. Others

like tea, coffee, theophylline etc.

2.Acting at loop of Henle

  1. Loop diuretics

Furosemide, torsemide, Ethacrynic acid

  1. Mercurial agents

Mercaptomerin

3.Acting at distal convoluted tubule

  1. Thiazides diuretics

 Chlorothiazide, chlorothalidone, Hydrochlorothiazide

  1. Sulfonamides

 Indapemide, Xipemide

4. Acting at collecting duct system

  1. K- sparing diuretics

. Aldosterone antagonist  Spironolactone

. Direct acting  Triamterene, amiloride

  1. ADH antagonists

Lithium salts, demeclocycline

OTHERS

 Na/K acetate

Na/K bicarbonate

Na/K Acetate

 Albumin

 Dextrose

V. Diuretics

1. General Considerations

A. These drugs promote a loss of Na+ and water from the body--increasing urine flow

B. Used for clinical management of many disorders

-Oedema, could be due to weak heart

-Hypertension

-Also used to reduce toxicity of substances--overdose

C. Drugs will alter kidney at

1) Proximal Loop

2) Loop of Henle

3) Distal Tubule

2 ) Drugs

A. Carbonic anhydrase inhibitors (first diuretics)- Acetazolamide

1. Inhibits enzyme carbonic anhydrase at proximal tubules

CA catalyzes in both directions

CA

HCO3 - + H+ ------ H2CO3 ------H2O + CO2

2. Inhibits HCO3 - (ie CO2 and H2O) reabsorption

3. Also inhibits Cl- reabsorption, this prevents Na+ reabsorption, (always together)

Thus decreased Na, Cl and bicarbonate reabsorption--less water reabsorbed

[Also low reabsorption of bicarbonate, therefore lose bicarb. in blood]

Weak diuretics- but used for treating glaucoma because aqueous humor has a lot of bicarbonate - decrease bicarbonate (eliminate in urine)----decrease pressure.

B. Loop agents

Inhibit NaCl reabsorption in thick ascending limb of loop of Henle

1. Furosemide (Lasix), Ethacrynic Acid [(like the Thiazides, they are sulfonamide derivatives--antibacterial agent produced diuresis)]

Inhibit ATPase pump- for Na+, K+, 2Cl-,

  • Normally pump out Na+, K+ and 2 Cl- - but K+comes back in - thus get positive lumen which drives Ca++ out, Furosemide blocks this - thus increased Ca++ excretion -- because no reabsorption (due to reduced positive potential across tubule therefore Ca++ is not driven out)

-Lasix - give to horses-give to bleeders-reduces edema formation -- race horses have developed very large hearts that produce high pressures -- the lungs can not take the high pressures and thus they bleed into the lungs (nose) -- Lasix reduces the bleeding

2. Pharmacokinetics- rapidly absorbed after oral administration

3. Therapeutic uses - most effective oral diuretics

used for treating acute edema (Pulmonary) and edema after congestive heart failure -- also used to treat hypercalcemia

4. Untoward Effects – lose K+ - later

C. Thiazides:

Benzothiadiazine, chlorothiazide, hydrochlorothiazide

Inhibit NaCl reabsorption in early segments of distal tubule- mechanism is unknown

There is a slight stimulation of Ca++ reabsorption

May stimulate active reabsorption -- controlled by parathyroid hormone

Drug is administered orally

Therapeutic uses: chronic edema, hypertension,kidney stones produced by calcium

Untoward effects

Lose K+

Secondary hyperaldosteronism due to fluid loss---turns on renin, angiotensin, aldosterone -- which in turn causes secretion of K+ - aldosterone leads to increased Na+ reabsorption and K+ secretion

D. Aldosterone antagonists- potassium sparing diuretics.

Spironolactone, Triamterene

Competitive antagonists of aldosterone

---Therefore interferes with aldosterone mediated Na-K exchange in distal tubule

Increase Na+ loss and decreases K+ loss

Used in combination with other diuretics to treat edema and hypertension

Administered orally