Nebivolol blocks β1- and β2-receptors, with many times greater selectivity for β1-receptors. A blockade of β1-receptors prevents endogenous ligands epinephrine and norepinephrine from binding to these receptors. These normally increase the frequency and force of the heartbeat. Blockade by nebivolol restores the abnormally increased heart rate to normal and allows the heart to pump blood more efficiently into the circulation. By blocking the β2-receptors, the smooth muscle of the blood vessels relaxes, resulting in a decrease in blood pressure. However, due to the high selectivity for β1-receptors, this effect is not very pronounced.
Absorption of nebivolol is not influenced by food intake. The maximum plasma level is reached after approximately 2-4 hours. The drug is 98% bound to serum albumin. Excretion occurs in both urine and stool. The half-life is about 12 hours.
Metabolism occurs in the liver and is catalyzed primarily by the enzyme CYP2D6. Due to genetic variations in the population, there are individuals who produce increased or decreased amounts of this enzyme. This can lead to considerable variations in the active ingredient in these individuals, which can influence the effect. Especially in the so-called "poor CYP2D6 metabolizers" (too little CYP2D6 present), increased plasma levels and thus increased undesirable side effects may occur after taking nebivolol. This particularly affects parts of the Caucasian population and individuals of African descent.
Simultaneous intake with substances that are also degraded by CYP2D6 or intake of substances that inhibit or induce CYP2D6 may lead to altered serum concentrations. This may result in increased side effects or a lack of effect.