Mechanism of Action and Advantages over ACE Inhibitors
Sartans act as direct antagonists of type 1 angiotensin II receptors (AT1). Unlike ACE inhibitors, which block only a single synthesis pathway in the vascular bed, AT1 receptor blockers eliminate the effects of angiotensin II comprehensively.
Angiotensin II can be formed not only systemically but also in tissues via alternative enzymatic pathways independent of ACE, and can also enter the bloodstream fully formed. Drugs of this group block receptors directly, eliminating the vasospastic action of angiotensin II regardless of its source.
Hemodynamic Effects and Influence on Hormonal Background
The pharmacological action of sartans on the cardiovascular system is realized through several key links:
- Direct blockade of vascular AT1 receptors prevents vasospasm.
- Reduction of total peripheral vascular resistance (systemic vascular resistance, SVR).
- Sustained blood pressure reduction.
- Action on the adrenal cortex, where receptor blockade leads to suppression of aldosterone secretion.
Clinical Application and Safety Profile
Due to their pharmacodynamics, sartans are widely used in clinical practice. The main indications for their prescription are arterial hypertension and chronic heart failure.
This class is characterized by excellent tolerability and a favorable safety profile. However, adverse reactions may still occur during pharmacotherapy:
- Central nervous system: headache, dizziness, general weakness.
- Allergic manifestations: a rare but dangerous complication is angioedema.