The beta-receptors located in the lung (called beta-2 receptors), when active or stimulated, produce relaxation of the muscle surrounding the bronchial tubes, which widens the bronchial passage (bronchodilatation). If these receptors are blocked from receiving nerve input, the reverse effect (bronchoconstriction) results. This may have devastating effects on patients with underlying bronchial asthma. One theory for the nature of asthma postulated that the disease represented a "blockage" of the beta-receptor that was either inherited or established through acquired illness. It is easy to see why using beta-blockers in patients with asthma has produced fatal asthma attacks. Beta-receptors are present in other organ systems such as the heart and circulation; these are referred to as beta-1 receptors. Beta-blockers that affect beta-1 receptors more than beta-2 receptors are termed "selective." These medications vary in potency and duration. A number of the selective beta-blockers produce less blockade of lung receptors, but there is still significant risk for exacerbating bronchial asthma. As a rule, all beta-blockers should be avoided by asthma patients. Don't Forget Eyedrops! Beta-blockers in the form of eyedrops are commonly used to treat glaucoma. Medication may be absorbed from the eye and delivered into the general blood circulation before reaching the bronchial tubes. Patients with bronchial asthma have suffered asthmatic attacks from beta-blockers introduced into the eye for treating glaucoma. Selective beta-blockers have been developed for glaucoma but may also produce bronchoconstriction. All patients with bronchial asthma should inform their ophthalmologists of their lung condition before treatment for glaucoma is initiated. In severe glaucoma cases where a beta-blockers is felt to be necessary, a selectine agent should be used and the patient's airflows closely monitored.Antidepressant Medication and B-Agonists Monoamine oxidase (MAG) inhibitors are commonly prescribed for depression. These drugs inhibit the enzyme responsible for breaking down epinephrine released from the adrenal gland. When a B-adrenergic agonist is administered to patients receiving a MAG inhibitor, there is a greater risk of adverse effects on the circulation, such as blood pressure elevation. This is more likely when the B-agonist is given by mouth or by injection since there is higher total-body absorption of the drug. By inhaling a B-agonist there is less chance of producing an adverse effect in a patient receiving a MAG inhibitor. When possible, an alternative antidepressant should be substituted in asthma patients to permit safe administration of a B-agonist. Patients who must receive both medications should be monitored closely for adverse circulatory effects. Sedatives and Asthma In asthma, as in other chronic illnesses, patients may experience increased levels of anxiety as well as sleeplessness. Requests for tranquilizers and sleeping pills are common. In patients with severe asthma, shortness of breath and fear of hospitalization may further heighten anxiety levels. Sleep may also be interrupted by asthmatic attacks. Why to Avoid Tranquilizers and Sleeping Pills All tranquilizers and sleeping pills affect the brain center that drives breathing. This reduces the activity of this vital center and causes more shallow breaths. Shallow breathing does not produce full expansion of the lung and results in lower oxygen levels. In patients with severe asthma, tranquilizers and sedatives may depress breathing which worsens attacks with possible life-threatening results. These patients should always avoid these agents.