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The **carbonic acid–bicarbonate buffer system** is the major physiological buffering mechanism for maintaining pH balance in human blood and tissues. It involves an equilibrium between dissolved carbon dioxide (CO₂), carbonic acid (H₂CO₃), bicarbonate ion (HCO₃⁻), and hydrogen ion (H⁺). This system is catalyzed by the enzyme carbonic anhydrase and operates according to the equation: CO₂ + H₂O ⇌ H₂CO₃ ⇌ HCO₃⁻ + H⁺. This buffer maintains blood pH tightly around 7.35–7.45, neutralizing excess acids or bases primarily via the interconversion of CO₂ (regulated by the lungs) and HCO₃⁻ (regulated by the kidneys). Dysfunction leads to acid–base disturbances such as metabolic acidosis/alkalosis and respiratory acidosis/alkalosis. Therapeutic manipulation typically targets components of this system, for example, by administering sodium bicarbonate or inhibiting carbonic anhydrase. This is **not a classical molecular target** like an enzyme, receptor, or ion channel, but rather a physiological system; therefore, it is inappropriate to consider it a direct drug target in the conventional sense. Additional notes: The term refers to a **chemical buffering system** rather than a discrete molecular entity (e.g., receptor, enzyme). Drugs may influence or interact with this buffer system, but it is not a molecular drug target itself. Issues may arise when extracting information for drug-target databases, as the system itself is broader than typical targets.
Modulation of blood bicarbonate levels; Inhibition of carbonic anhydrase (affecting equilibrium between CO₂, carbonic acid, and bicarbonate)
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