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Overuse of β 2 agonists and asthma treatment without proper inhaled corticosteroid use has been associated with an increased risk of asthma exacerbations and asthma-related hospitalizations. [8] The excipients, in particular sulfite, could contribute to the adverse effects.
In general, pure beta-adrenergic agonists have the opposite function of beta blockers: beta-adrenoreceptor agonist ligands mimic the actions of both epinephrine- and norepinephrine- signaling, in the heart and lungs, and in smooth muscle tissue; epinephrine expresses the higher affinity.
The proposed mechanism is that while LABAs relieve asthma symptoms, they can also promote bronchial inflammation and sensitivity without warning. [23] On February 18, 2011, the FDA issued a safety alert for long-acting β agonists. [24]
The combination of beta blockers and antihypertensive drugs will work on different mechanism to lower blood pressure. [17] For example, the co-administration of beta-1 blocker atenolol and ACE inhibitor lisinopril could produce a 50% larger reduction in blood pressure than using either drug alone. [18]
Non-selective beta blockers In some cases, exacerbation of asthma or COPD , and erectile dysfunction are also reported. [ 10 ] For examples, certain non-selective beta blockers, such as carvedilol , can cause edema , and sotalol can block potassium channels in the heart, leading to QT prolongation and an increased risk of torsades de pointes .
By treating asthma with optically pure (R)-salbutamol the risk of side effects, such as nervous system stimulatory effects and cardiac arrhythmia, can be minimized. [20] There are several routes for enantioselective synthesis , as well as methods for synthesis of the racemic mixture followed by chiral resolution .