Drugs
Among the beta-blockers there are many different drugs, all of which have the same mechanism of action with some peculiarities and for this reason are used in different diseases. The active ingredients bisoprolol and metoprolol are the best-known beta-blockers for the treatment of high blood pressure and the secondary prevention of heart attacks. – Bisoprolol is usually taken in a dosage of 2.5 mg or 5 mg once a day.
- Metoprolol is available as mite (47.5 mg) or as Belok zok (95 mg). – Nebivolol is used slightly less frequently, but is approved exclusively for the treatment of high blood pressure. – Propanolol is mainly used to treat high blood pressure or rapid heart rate.
- Atenolol is a drug that is used mainly in emergencies for the treatment of myocardial infarction or the very rapid transition disorder (tachycardia) and in this case is injected via the vein. The second major area of application for beta-blockers is the reduced production of aqueous humor in glaucoma. In this case beta-blockers are used as eye drops, which should usually be administered 2-3 times into the affected eye.
The most important substances are: Although the systemic effect of beta-blockers in eye drops is reduced, it is still present. Thus, the use of these eye drops can also lead to a reduction in pulse rate and blood pressure. – Betaxolol
- Timolol
- Carteolol and
- Pindolol
Fields of application
The main area of application for beta-blockers is high blood pressure and cardiac arrhythmia. It is assumed that adrenergic messenger substances, which are sometimes more and sometimes less released by the body, bind to the heart and both accelerate the heartbeat and increase blood pressure. Physiologically, these substances are always released by the body when an increased cardiac output and a stronger heartbeat is required.
As a rule, these are physical strains that make such physiological changes necessary. During running and physical exertion, more blood would be required from the body in a shorter time. Adrenaline and noradrenaline are therefore released to increase the heartbeat and blood pressure via the beta-receptors.
In the case of pathological high blood pressure, one takes advantage of this mechanism of action and blocks the beta-receptors with a blocker. Even if adrenergic messenger substances are now released by the body, they can no longer bind to the receptors and produce the physiological effect of high blood pressure and increased frequency. In the case of pathological high blood pressure or cardiac arrhythmia, two theories are assumed, which is why beta receptors trigger this clinical picture.
On the one hand, it is assumed that the messenger substances are released without a specific reason and thus develop a physiological effect at the receptors without being necessary. It is also assumed that in people suffering from high blood pressure or cardiac arrhythmia the receptor system is hypersensitive and is stimulated even at low levels of the messenger substance. Although beta-blockers are not necessarily the first choice for treating hypertension, they are above all a combination alternative with other hypertension drugs.
When used, the active substance attaches itself to the receptors and blocks them, the messenger substances can no longer attach and develop their effect. As a result, blood pressure and heart rate drop. Cardiac arrhythmias are rapid transmissions in the heart muscle that are stimulated by adrenaline and noradrenaline.
If the receptors are blocked, the transmission of stimuli is also reduced, resulting in a lower and more regular pulse. The production of aqueous humor in the eye is also mediated by beta-receptors. In glaucoma there is a pathological increase of the aqueous humor in the eye and thus an increase in intraocular pressure.
This can lead to damage to the optic nerve over a longer period of time. Here too, the effect of the receptor blockade is used. At the moment when the substance binds to the receptor, the actual physiological effect of the messenger substances can no longer be triggered.
In this case the intraocular pressure decreases. The opposite effect of the beta-blockers is used in asthma-bronchiale. Since the binding of the messenger substances leads to an expansion of the bronchial tubes, the use of beta-blockers would lead to a contraction of the bronchial tubes.
For this reason beta-blockers should not be used in asthmatics. Here, receptor stimulants are used to stimulate the receptor on the lungs (and everywhere else in the body). The so-called beta-blockers cause bronchial dilatation in the lungs (especially in bronchial asthma) and an increase in heart rate in the heart (unwanted effect). The use of beta-blockers is therefore contraindicated in asthmatics.
