Beta-Receptor Stimulating Drugs, Part 2 Print E-mail



Beta-2 Specific Stimulating Drugs

Happily, though, it turns out that there is more than one type of beta-receptor. Beta-1 receptors are abundant in the heart, and activating them causes the heart to beat more quickly and forcefully. Beta-2 receptors are the primary ones in the airways, and their activation causes bronchodilation. Pharmaceutical research is now looking for cardiac medication that blocks beta-1 receptorsto prevent the heart from beating too fastand has no effect on beta-2 receptors. The goal for bronchodilator drugs is potent beta-2 stimulation with minimal beta-1 action.

Currently, there are six major "beta-2 selective" bronchodilators available. Although they vary in potency and duration of action, they all last longer than isoproterenol and their cardiac effects are less pronounced. Five have been available for a while. They are isoetharine, metaproterenol, terbutaline, albuterol (known as salbutamol everywhere except in the United States), and bitolterol. The sixthsalmeterolhas recently become available. Studies comparing it to the earlier five indicate that it is even more beta-2 selective, more potent, and longer-acting. Although it takes longer to reach its maximum bronchodilation effect, it lasts for 12 hourstwice as long as the others. It's not a substitute for them, however. The current recommendation is to use salmeterol on a regular twice-a-day maintenance schedule, and use albuterol as a "rescue" drug to relieve an acute bronchospasm.

It has been observed that beta-2 receptors in airway muscle lose sensitivity after a patient begins using a beta-stimulator drug. This explains the noticeably decreased effectiveness of these drugs over the first several weeks of use. After this initial change, though, response to the drug becomes relatively stable. This sensitivity loss is the body's attempt to reduce what it perceives as overstimulation of the beta-receptors. It reacts by actually decreasing their number. We are not aware, though, of any studies that suggest increasing the dosage of beta-2 stimulating drugs to counter this loss of sensitivity. (The long-term implications of this phenomenon for the patient are not yet clear.)

Administration: The effectiveness of these drugs is partly determined by how they are taken: orally, by injection, or by inhalation. Inhalationwhich is the most commonhas two big advantages: (1) because the drug is deposited directly in the airways, less of the drug is needed for a given result than when it has to be distributed throughout the body to reach the airways; and (2) because less of the drug travels throughout the body, the side effects are lessened. But inhalation also has two disadvantages: (1) because the drug lands primarily in the large airways, the dilation benefit is concentrated in the central airways; and (2) a severe respiratory obstruction prevents inhaled drugs from reaching obstructed airways (but oral and injected medication will, because they travel in the blood).

Interactions

Theophylline: Beta-2 stimulators and theophylline are often used together. In combination they act synergistically, meaning that the presence of each one makes the other more effective. Because of this synergistic action, the dose of each can be reduced when they are combined. And the combination often achieves greater bronchodilation than the higher dose of either drug alone, plus the lower doses make side effects less severe.

Cortico'steroids: These anti-inflammatory drugs intensify beta-2 effects by raising beta-2 receptor sensitivity, possibly by increasing their numbers.

Monoamine Oxidase (MAO) Inhibitors: These drugs are used in the medical treatment of severe emotional depression. Since they inhibit the enzyme that would otherwise destroy excess adrenaline, the concentration in the body of this natural beta-receptor stimulator becomes much greater than usual. Caution is advised in considering the use of oral beta-stimulators for COPD patients already taking MAO inhibitors because of possible intensification of cardiovascular effects from adding a synthetic beta-stimulator to an already high concentration of adrenaline.

Beta-Blocking Drugs: Beta-blockers (designed to inactivate beta-1 receptors) are increasingly popular for treating cardiovascular disorders. In sufficient doses, though, they block the effects of beta-2 stimulators. For the COPD patient who has developed a significant asthma component, the result can be dangerous. This strongly applies to the nonspecific beta-1 blockers (for example, propranolol, nadolol, pindolol, timolol), and somewhat less to the specific beta-1 blockers (for example, metroprolol, atenolol). Even when used as a topical eye medication (Timoptic) for the treatment of glaucoma (a potentially blinding eye disease), enough of the beta-blocking agent can be absorbed into the blood to cause clinically significant bronchospasm. When at all possible, every attempt should be made to exclude use of beta-blocking medication with COPD patients who have a significant asthma component.

Make it a rule to clear any medicationincluding over-the-counter drugswith the doctor treating your COPD before you use them. This becomes especially important to remember if you are seeing more than one doctor, because then the chance increases of being on conflicting medications. Such common problems as anxiety, insomnia, indigestion, and hypertension require especially careful management to avoid discomfort or hazard from drug interactions.


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