DEPENDENT EDEMA AND CALCIUM CHANNEL BLOCKADE: A CRITICAL ANALYSIS OF VASCULAR RESPONSES TO AMLODIPINE

Abstract

Peripheral edema associated with the use of calcium channel blockers, such as amlodipine, is a common complication in the treatment of arterial hypertension, especially in elderly patients. This adverse effect occurs due to selective vasodilation of arterioles, which is not accompanied by corresponding venous dilation, resulting in increased capillary hydrostatic pressure and fluid leakage into the interstitial space. This process leads to fluid accumulation, mainly in the lower extremities. Aging exacerbates this condition, as there is a natural decline in the efficiency of the lymphatic and venous systems, often compromised by comorbidities such as venous insufficiency and cardiac dysfunction. In addition to hemodynamic factors, the response to amlodipine may be modulated by individual genetic characteristics, particularly variations in the gene responsible for metabolizing the drug. Patients with certain genetic predispositions metabolize amlodipine more slowly, which can increase plasma concentrations and intensify side effects, such as edema. To mitigate these effects, alternatives such as dose adjustments, the concomitant use of diuretics, or substitution with other antihypertensive agents, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs), can be effective. Understanding the physiological and genetic mechanisms that predispose patients to edema is crucial for optimizing hypertension treatment and minimizing complications, especially in higher-risk populations like the elderly.