Potassium-sparing diuretics are one of the most commonly used drugs for heart, kidney and liver diseases, which are accompanied by edema.
The mechanism of action potassium-sparing diuretics. The mechanism of action is quite difficult to understand, but it is important for choosing the type of diuretic. Potassium-sparing diuretics, disrupting Na + reabsorption, interfere with the depolarization of the apical membrane of the main nephrocytes, which leads to a delay of K + in the blood. Diuretics also reduce the secretion of H + proton ATPase intercalated nephrocytes. The diuretic effect of potassium-sparing agents is weak since a small amount of Na + is reabsorbed in the distal parts of the nephron. The preparations increase the excreted fraction of Na + only up to 3 – 5%, moderately increase the excretion of Cl-, retain K +, H + and Mg2 + in the body, change the blood flow in the kidneys and filter little. When administered together with potent diuretics and thiazides, potassium-sparing diuretics eliminate compensatory enhancement of Na + reabsorption in the distal nephron and also eliminate hypokalemia.
Preparations of this group are divided into aldosterone antagonists and sodium channel blockers. Today we will talk about aldosterone antagonists
Aldosterone increases the reabsorption of Na + and stimulates the secretion of K +, so there is edema. It contributes to the development of edema.
The most commonly used antagonist aldosterone steroid structure – SPIRONOLACTON (Aldactone). This drug is competitively bound to mineralocorticoid receptors in nephrocytes. The complex “spironolactone-receptor” does not possess biological activity.
Against the background of the action of spironolactone permeability and the number of sodium channels, the function of Na +, K + -ATP-ase and its energy supply are reduced. The diuretic effect of spironolactone is expressed with a high concentration of aldosterone in the blood and develops only 2 – 3 days after the start of the course therapy. A long latency period is needed for the destruction of previously synthesized AIP (aldosterone-induced proteins).
Spironolactone, weakening the activating effect of aldosterone on the synthesis of fibrous tissue in the heart, strengthens heart contractions, facilitates relaxation of the heart in diastole, and prevents ventricular arrhythmias caused by a circular wave of excitation. Moderately reduces blood pressure and heart afterload.
Indications for use spironolactone (Aldactone) following:
- Primary hyperaldosteronism, or Conn’s syndrome (tumor or bilateral hyperplasia of the adrenal cortex);
- Secondary hyperaldosteronism (increased aldosterone secretion in heart failure);
- Systolic and diastolic heart failure;
- Arterial hypertension;
- Hypokalemia;
- Hyperandrogenesis in women.
Side effects:
- Hyperkalemia;
- Metabolic acidosis;
- Gynecomastia and impotence in men, coarsening of the voice and menstrual abnormalities in women (effects on sex hormone receptors);
- Diarrhea, gastritis, peptic ulcer of the stomach, complicated by bleeding
- Headache, tremor, ataxia;
- Skin rash, thrombocytopenia.
Spironolactone enhances the therapeutic effect of cardiac glycosides.
Contraindications:
Hypersensitivity, Addison’s disease, hyperkalemia, hypercalcemia, hyponatremia, chronic renal failure, anuria, liver failure, diabetes, metabolic acidosis, menstrual disorders or breast enlargement.