Pulmonary effects of nebivolol

Abstract

The pharmacological control of arterial hypertension is a very frequent issue in clinical practice and some critical aspects can arise in particular circumstances and with particular molecules. In the case of hypertensive subjects with respiratory comorbidities, when first introduced, these β-adrenergic receptor antagonists were described as affecting airway patency as a result of their antagonism against β2-adrenergic receptors within airway muscles. New molecules with a better respiratory tolerability were subsequently designed in order to overcome the narrow therapeutic window of first-generation β-adrenergic receptor antagonists. Nebivolol is a third-generation β-adrenergic receptor antagonist with high β1-selective adrenergic receptor antagonism and vasodilating properties that induces a substantial decrease of arterial pressure in hypertensive subjects while preserving their left ventricular function. Respiratory effects of nebivolol have been investigated in animal models, in healthy volunteers and in clinical trials carried out on patients suffering from bronchial asthma and chronic obstructive pulmonary disease (COPD). In contrast to older compounds, nebivolol, which modulates the endogenous production of nitric oxide and affects oxidative cascade, proved clinically well tolerated in terms of respiratory outcomes in this type of subject. Moreover, due to the substantial dissociation between its cardiac and pulmonary activity, nebivolol confirmed a very good safety profile when regularly administered to hypertensive subjects with obstructive respiratory comorbidities.