Beta blocker | Medicines for high blood pressure

Beta blocker

Beta-blockers are indispensable, especially for patients with a weak pumping of the heart (=heart failure) or for patients after a heart attack. Beta-blockers take their name from receptors on the heart. Receptors are something like translators of cells and organs.

Messenger substances dock on them and cause a predetermined change. The so-called beta-receptors are located, among other things, on the heart. They receive signals from our vegetative nervous system, here the so-called sympathetic nervous system.

It is activated during physical exertion and stress and makes our body more efficient. It increases the heart rate at the heart and makes it beat more strongly. It expands the bronchial tubes so that we can breathe better and it inhibits intestinal activity to provide as much energy as possible for performance.

The signals of the nervous system are received and converted by various receptors/translators. A distinction is made between alpha and beta receptors (Greek term for the letters A and B). Alpha receptors are located, among other things, on the vessels and cause constriction, while beta receptors are mainly found on the lungs and heart.Beta blockers prevent the action of the driving sympathetic nervous system by blocking the beta receptor for its transmitter.

As a result, the heart beats less quickly and strongly. If the heart beats slower and less strongly, less blood is pumped into the vascular system and blood pressure may drop. In addition to the beneficial effect on high blood pressure, beta-blockers also have the great advantage of reducing the oxygen consumption at the heart by beating slower and less vigorously, because less work means less energy consumption.

This benefits patients with diseases of the coronary vessels (=vessels that supply the heart and lie around it like a wreath), because in these patients the vessels are no longer able to transport enough blood to the heart muscle due to calcification, resulting in a lack of blood flow and, last but not least, heart attacks. Special caution in the therapy with beta blockers is required in patients with asthma or other obstructive lung diseases such as COPD. Since the receptors of the heart are also found in a similar variant on the lungs, stimulation of the receptors can, in addition to the effect on the heart, also trigger an attack of breathlessness, since the airways become narrower due to the blockage of the beta receptors.

In further development, therefore, more selective beta-blockers have been developed which, in lower doses, have a greater effect on the heart than on the lungs, thus usually ruling out this complication. Examples of these so-called cardioselective (cardio=heart) beta blockers are metoprolol and atenolol. Besides the asthma attack, the most important side effects of all beta-blockers are weight gain at the beginning of treatment, disorders of male potency, drops in blood pressure up to circulatory collapse, an increase in cholesterol levels and an increase in the risks of diabetes mellitus.

Diabetes or a heart beating permanently too slowly (= bradycardias) are therefore contraindications against taking a beta-blocker. Beta-blockers are often identified by the suffix “-olol” in the name of the active substance. ACE inhibitors attack a completely different mechanism of the body.

ACE inhibitors get their name from an enzyme that they block at work, the AC enzyme (=angiotensin-converting enzymes). This enzyme causes the release of a substance in the body that constricts the blood vessels, the so-called angiotensin, which is known as “vascular tensioner”. Since the ACE inhibitors block this AC enzyme and thus fewer vasoconstricting substances are produced, the vessels remain wide and blood pressure cannot rise too high.

Since the effect depends on the activity of the enzyme, the effect of an ACE inhibitor is often difficult to predict. Therapy should therefore be started at low doses and under medical supervision. The activity of the enzyme is particularly high when diuretics are administered at the same time.

Here, the effect of an ACE inhibitor will be very strong. A combination therapy of these drugs should therefore only be started very carefully. In addition to this effect on the blood vessels, ACE inhibitors also have a beneficial effect on the course of heart failure.

In this pumping weakness of the heart, they prevent a remodelling process that makes the heart increasingly inefficient. A frequent complication of the therapy is a dry irritable cough, which about 5-10% of the treated patients get. Since this phenomenon is not limited to a single active substance from the group of ACE inhibitors, a change of the active substance is not advisable, but a complete switch to another class of antihypertensives is indicated.

In most cases, the therapy is then selected with the help of an AT1 blocker. Skin rashes and swelling, so-called edema, kidney dysfunction and severe drops in blood pressure can also occur during treatment with ACE inhibitors. ACE inhibitors are not allowed in cases of kidney damage, heart valve defects or during pregnancy.

In these cases, other preparations must be used. The best-known members of the ACE inhibitor group are captopril, the original substance of ACE inhibitors, enalapril, a more effective and longer-lasting preparation. Newer preparations have an even longer duration of action, so that of the three times daily administration of captopril and the two times daily administration of enalapril, only a single administration is required each day. The representatives of the ACE inhibitors can be recognized by the word ending “-pril” at the end of the active substance name.