Alpha-adrenergic block type medications used for hypertension:
List of beta-adrenergic blocking drugs used in the treatment of arterial hypertension:
- Azoprol Retard;
Xalac is a popular combination drug that helps to eliminate the patient’s problem.
Alpha-beta-blocking medications are:
These substances create a persistent non-competitive block that protects the corresponding structures. In time, it optimally functions up to half a day. Such blockers counteract adrenaline more than thirty times more effective than norepinephrine. This determines the choice of these drugs when they are used in therapeutic regimens against the background of an increased concentration of adrenaline.
Among α-blockers, two main subgroups are distinguished.
The first of them includes the so-called selective adrenergic blockers, that is, those that selectively act on α1-adrenergic receptors.
The second class includes non-selective substances, that is, substances that act on both a-1 and a-2-adrenergic receptors.
It is non-selective blockers that are used to relieve acute attacks (crises) of hypertension. For long-term use, these drugs are mainly not intended. It makes sense to think about the appointment of drugs in this group when the readings of the tonometer indicate the numbers 90/145 mm RT. Art.
Treatment with these adrenergic blockers is justified if GB is accompanied by:
- Corneal diseases of the eye;
- Vestibular apparatus dysfunctions;
- Impaired normal peripheral circulation;
- Neurotic conditions
- Optic nerve ischemia;
- Heart pathology in the form of heart failure;
- Wounds caused by frostbite and pressure sores;
- Diabetes mellitus in hyperadrenal form;
- Meniere’s Syndrome;
- Trophic ulcers.
What drugs, representing the most popular alpha-blockers and prescribed by doctors for hypertension, are specialists most often paying attention to?
- Alfuzosin. The drug has proven itself in schemes involving prostatitis in the patient’s history or the presence of a disease such as hypertrophy of myocardial tissue.
- Clonidine. A powerful antihypertensive drug that relieves OPSS. It counteracts somatovegetative alkaloids poisoning and opium withdrawal. It has a painkiller effect on the central nervous system.
- Dopegit. Despite the fact that this medicine causes drowsiness, its use in the acute phase of jumps. Blood pressure is quite effective and justified.
- Nicergoline. It is optimal in the treatment of not only GB, but also with problems with peripheral blood flow. Of the side effects characteristic of this drug, sleep disorder is noted.
- PROROXANE They treat differences in high blood pressure with concomitant atherosclerosis of blood vessels.
- Phentolamine It has proven itself in the treatment of high blood pressure, accompanied by pathological processes occurring in the soft tissues of the limbs. It is probably the most popular non-selective alpha blocker. In relation to the heart, it is a nootropic drug. Great for stopping hypertensive crises.
- Urapidil. It requires close monitoring during use, as it is capable of extremely sharply lowering blood pressure up to threshold levels. A concomitant disease, which often determines the choice of this drug, is impotence: Urapidil helps restore erectile ability.
- Yohimbine. Similar to previous drug. It has adverse reactions in the form of urination disorders in male patients.
- Prazosin. Refers to selective blockers. It is distinguished by the possibility of use in heart failure in its stagnant form. An undoubted advantage is that the drug has a pronounced ability to lower bad cholesterol.
- Doxazosin. It has the ability to prolonged action. It is important that the drug lowers the patient’s blood pressure not only at rest, but also during physical activity. The concentration of norepinephrine this drug leaves unchanged. Adrenaline, serotonin and dopamine are practically unchanged. In relation to the formed elements of the blood has a pronounced ability to perform anti-aggregation function.
Here, in short, which drugs for high blood pressure, which are alpha-adrenergic blockers, are most often used in clinical practice.
- The mechanism of action of beta-blockers
- Alpha-adrenergic blockers: features of work
- Classification of beta-blockers
- Cardioselectivity of beta-blockers
- Beta blockers: contraindications
- Incompatibility with other drugs
- Feedback and recommendations
- Beta blockers: side effects
- Which beta blocker is better?
- Beta blocker withdrawal syndrome
The mechanism of action of beta-blockers
The mechanism of action of drugs of this group is due to their ability to block beta-adrenergic receptors of the heart muscle and other tissues, causing a number of effects that are components of the mechanism of the hypotensive effect of these drugs.
- Reduced cardiac output, heart rate and heart rate, resulting in reduced oxygen demand for the myocardium, increased number of collaterals and redistributed myocardial blood flow.
- Heart rate reduction. In this regard, diastoles optimize the total coronary blood flow and support the metabolism of the damaged myocardium. Beta-blockers, “protecting” the myocardium, are able to reduce the area of myocardial infarction and the frequency of complications of myocardial infarction.
- Decrease in total peripheral resistance by reducing renin production by the cells of the juxtaglomerular apparatus.
- Decreased release of norepinephrine from postganglionic sympathetic nerve fibers.
- Increased production of vasodilating factors (prostacyclin, prostaglandin e2, nitric oxide (II)).
- Decreased reverse absorption of sodium ions in the kidneys and the sensitivity of baroreceptors of the aortic arch and carotid (carotid) sinus.
- Membrane-stabilizing effect – a decrease in the permeability of membranes for sodium and potassium ions.
Along with antihypertensive beta-blockers have the following actions.
- Antiarrhythmic activity, which is due to their inhibition of the action of catecholamines, a slowdown in sinus rhythm and a decrease in the speed of impulses in the atrioventricular septum.
- Antianginal activity – competitive blocking of beta-1 adrenergic receptors of the myocardium and blood vessels, which leads to a decrease in heart rate, myocardial contractility, blood pressure, as well as to increase the duration of diastole, improve coronary blood flow. In general, to reduce the oxygen demand of the heart muscle, as a result, tolerance to physical activity increases, periods of ischemia are reduced, the frequency of anginal attacks in patients with exertional angina and post-infarction angina is reduced.
- Antiplatelet ability – slow down platelet aggregation and stimulate prostacyclin synthesis in the endothelium of the vascular wall, reduce blood viscosity.
- Antiox >
Beta-adrenoreceptor stimulation effects
From the table it becomes clear that beta-1 adrenergic receptors are located mainly in the heart, liver and skeletal muscle. Catecholamines, affecting beta-1 adrenergic receptors, have a stimulating effect, resulting in an increase in heart rate and strength.
Alpha-adrenergic blockers: features of work
Consider the features of the work of this type of blockers that are manifested in relation to some systems of the human body. Let’s start with the cardiovascular system.
So, alpha-adrenergic blockers have a pronounced relaxing effect in relation to precapillary sphincters, arterioles and veins. Arteries are less affected by these substances. The fall in OPSS leads to a decrease in blood pressure. This leads to a decrease in the load on the heart muscle and prevents its possible heart attack.
Of the negative consequences, it is worth noting the possibility of developing orthostatic hypotension and, possibly, tachycardia.
The organs of vision for suppressing receptors with the use of α-1 adrenergic blockers may well respond with pupil myosis.
The digestive system responds with an increase in secretory function and peristalsis.
It is contraindicated to use antihypertensive drugs of this type, if there is:
- Severe hypotension;
- Narrowing of the lumen of the aorta;
- Stomach ulcer.
Of course, the expected negative effects caused by these drugs. Here are the most characteristic of them:
- Orthostatic collapse;
- Stool disorders;
- The narrowing of the pupil.
Classification of beta-blockers
Depending on the predominant effect on beta-1 and beta-2, adrenergic receptors are divided into:
- cardioselective (Metaprolol, Atenolol, Betaxolol, Nebivolol);
- cardioselective (Propranolol, Nadolol, Timolol, Metoprolol).
Beta-blockers are pharmacokinetically divided into three groups, depending on their ability to dissolve in lipids or water.
- Lipophilic beta-blockers (Oxprenolol, Propranolol, Alprenolol, Carvedilol, Metaprolol, Timolol). When applied orally, it is rapidly and almost completely (70-90%) absorbed in the stomach and intestines. Preparations of this group penetrate well into various tissues and organs, as well as through the placenta and the blood-brain barrier. As a rule, lipophilic beta-blockers are prescribed in low doses for severe hepatic and congestive heart failure.
- Hydrophilic beta-blockers (Atenolol, Nadolol, Talinolol, Sotalol). Unlike lipophilic beta-blockers, when used internally, they are absorbed only by 30-50%, are metabolized to a lesser extent in the liver, and have a long half-life. They are excreted mainly through the kidneys, and therefore hydrophilic beta-blockers are used in low doses with insufficient renal function.
- Lipo- and hydrophilic beta-blockers, or amphiphilic blockers (Acebutolol, Bisoprolol, Betaxolol, Pindolol, Celiprolol), are soluble in lipids and water, after application, 40-60% of the drug is absorbed inside. They occupy an intermediate position between lipo- and hydrophilic beta-blockers and are excreted equally by the kidneys and liver. Drugs are prescribed for patients with moderate renal and hepatic insufficiency.
- Cardiac-selective (Propranolol, Nadolol, Timolol, Oxprenolol, Pindolol, Alprenolol, Penbutolol, Carteolol, Bopindolol).
- Cardioselective (Atenolol, Metoprolol, Bisoprolol, Betaxolol, Nebivolol, Bevantolol, Esmolol, Acebutolol, Talinol).
- Beta-blockers with the properties of alpha-adrenergic receptor blockers (Carvedilol, Labetalol, Celiprolol) are drugs that have inherent mechanisms of the hypotensive effect of both groups of blockers.
Cardioselective and non-cardioselective beta-blockers, in turn, are divided into drugs with and without internal sympathomimetic activity.
- Cardioselective beta-blockers without internal sympathomimetic activity (Atenolol, Metoprolol, Betaxolol, Bisoprolol, Nebivolol) along with antihypertensive effect reduce heart rate, give antiarrhythmic effect, do not cause bronchospasm.
- Cardioselective beta-blockers with internal sympathomimetic activity (Acebutolol, Talinolol, Celiprolol) reduce heart rate to a lesser extent, inhibit the automatism of the sinus node and atrioventricular conduction, give a significant antianginal and antiarrhythmic effect in case of sinus tachycardia, little and supraventricular, supraventricular, and supraventricular -2 adrenergic receptors of the bronchi of the pulmonary vessels.
- Non-cardioselective beta-blockers without internal sympathomimetic activity (Propranolol, Nadolol, Timolol) have the greatest antianginal effect, so they are often prescribed for patients with concomitant angina pectoris.
- Non-cardioselective beta-blockers with internal sympathomimetic activity (Oxprenolol, Trazicor, Pindolol, Wisken) not only block, but also partially stimulate beta-adrenergic receptors. Drugs of this group to a lesser extent reduce heart rate, slow atrial-ventricular conduction and reduce myocardial contractility. They can be prescribed to patients with arterial hypertension with a mild degree of conduction disturbance, heart failure, and a rarer pulse.
Cardioselectivity of beta-blockers
Cardioselective beta-blockers block beta-1 adrenergic receptors located in the cells of the heart muscle, juxtaglomerular apparatus of the kidneys, adipose tissue, the cardiac conduction system and intestines. However, the selectivity of beta-blockers is dose dependent and disappears with large doses of beta-1 selective beta-blockers.
Non-selective beta-blockers act on both types of receptors, beta-1 and beta-2 adrenergic receptors. Beta-2 adrenergic receptors are located on the smooth muscles of blood vessels, bronchi, uterus, pancreas, liver and adipose tissue. These drugs increase the contractile activity of the pregnant uterus, which can lead to premature birth.
Cardioselective beta-blockers have an advantage over non-cardioselective in the treatment of patients with arterial hypertension, bronchial asthma and other diseases of the bronchopulmonary system, accompanied by bronchospasm, diabetes mellitus, intermittent claudication.
Let us make some comparison of the hemodynamics of drugs that are α and β-blockers.
- Heart rate. α-blockers smoothly increase this indicator, in contrast to quite quickly reducing the pulse of β-blockers.
- Both types of blood pressure definitely lower blood pressure.
- The atrioventricular conduction of the impulse from the synotrial node to the ventricle of the heart leaves α-blockers unchanged, and β-blockers significantly lower.
- Myocardial contractility under the action of drugs represented by α-blockers remains unchanged or increases slightly. β-adrenergic blockers slightly lower this indicator.
- Both types of blockers lower total peripheral vascular resistance, and α-blockers do this more explicitly.
- The effect on the renal blood flow is exactly the opposite: α-blockers enhance this indicator, and β-blockers act as their antagonists.
In the clinical manifestations of these types of adrenergic blockers, there is also a similarity, and some difference.
Acting on blood pressure, both of these types lowered the systolic pressure border by 6 points. In relation to the diastole phase, the pressure decreased by 4 marks. Heart rate dropped by 5 beats per minute. All these data relate to patients exposed to hypertension in mild to moderate form.
With an increase in the dose of the drugs, in both cases the heart rate dropped significantly, but the dynamics of pressure reduction remained practically unchanged.
Beta blockers: contraindications
- essential arterial hypertension;
- secondary arterial hypertension;
- signs of hypersympathicotonia (tachycardia, high pulse pressure, hyperkinetic type of hemodynamics);
- concomitant coronary heart disease – angina pectoris (smokers selective beta-blockers, non-smokers – non-selective);
- heart attack, regardless of the presence of angina pectoris;
- heart rhythm disturbance (atrial and ventricular extrasystole, tachycardia);
- subcompensated heart failure;
- hypertrophic cardiomyopathy, subaortic stenosis;
- mitral valve prolapse;
- risk of ventricular fibrillation and sudden death;
- arterial hypertension in the preoperative and postoperative period;
- beta-blockers are also prescribed for migraines, hyperthyroidism, alcohol and drug withdrawal.
From the cardiovascular system:
- atrioventricular blockade of 2-3 degrees;
- acute heart failure;
- cardiogenic shock;
- vasospastic angina.
From other organs and systems:
- bronchial asthma;
- chronic obstructive pulmonary disease;
- stenosing disease of peripheral vessels with limb ischemia at rest.
The use of each type of blocker is based on the specifics of their effect:
- Alpha-blockers are used as a vasodilator, leading to a decrease in pressure, reduction of spasmodic processes.
- Beta-blockers for hypertension are used to slow down the heart rhythm, which leads to a decrease in blood pressure through exposure to the sinus node. The effect also affects the peripheral part of the vascular system, leading to its narrowing.
- Alpha-β-blockers are used in therapy requiring a combined effect – vasodilation with a simultaneous slowdown of the heartbeat.
Incompatibility with other drugs
When prescribing a comprehensive treatment of any disease, three probabilistic lines of development of drug interactions are possible. So this can be a mutual enhancement of the positive therapeutic effect of both one of the drugs involved in the medical scheme, and their general effect on the body.
- Perhaps a neutral, indifferent attitude of drugs to each other during treatment.
- Possible inhibition of the action of any drugs under the influence of other drugs used.
- Their dangerous combinations are possible.
Consider such dangerous cases.
- The combination of beta-blockers with antihypertensive drugs of the nonhydropyridone group of calcium channel blockers. Recall that these are Verapamil, Nifedipine, Isoptin and the like. The use of a drug of either of these two classes in itself leads to a drop in heart rate. The erroneous purpose is dangerous because the combined effect of the combined calcium channel blockers and adrenergic blockers leads to a critical slowdown in heart rate. The only justified case of the need for such a combination is the control of the rhythm of the ventricles against the background of stable inconsistency in the work of the heart departments.
- The combination of beta-blockers with centrally acting drugs. The group of CD drugs includes drugs that affect the sympathetic activity of the brain. This is Guangfacin, Clonidine, Methyldopa. The danger is a mutual increase in side effects with a combination of adrenergic blockers with these drugs.
Feedback and recommendations
Employees BOU VPO MGMSU (Moscow) Evdokimov V., Markova L.I. they write: “Hypertension is a critical risk factor. Nevertheless, adequate comprehensive treatment with beta-blockers can not only reduce neurological problems, but also significantly improve the prognosis for recovery and improve the quality of life of the patient. This is confirmed by the clinical use of drugs of the bisoprolol group (Concor, Takeda and the like). ”
Based on the analysis of randomized clinical trials, the so-called “Cochrane reviews” (Wong GWK, Laugerotte A, Wright JM) note: “Any subclasses of beta-blockers equally lower the boundaries of both systolic and diastolic pressure. Unlike other types of antihypertensive drugs, they have no (or minimal) effect on pulse pressure. ”
In the work on this article, scientific materials provided by scientists from the Moscow State Medical-Dental University were used. Let’s try, based on the work of these scientists, to summarize the data that we presented above.
In short, both alpha-blockers and beta-blockers are able to simultaneously block two types of adrenergic receptors. Drugs of this class are quite competitive with other antihypertensives.
Taking into account the results of studies conducted by MOSES, PROGRESS and similar companies, we can safely say that the therapeutic use of beta-blockers for the treatment of hypertension reduces the risk of stroke by 40%.
In relation to the central nervous system, the prolonged use of such drugs is potentially able to restore the self-regulation of cerebral vessels. This applies to the early stages of hypertension and vascular pathologies of this section of the central nervous system.
Practical medicine in the clinical use of this type of antihypertensive drug relies mainly on beta-1-selective drugs. They are almost devoid of such undesirable side effects as bronchospasm, vasoconstriction, increased OPSS. And these processes often lead to a violation of metabolic functions involving carbohydrates and lipids.
The most popular selective beta-blocker, which is currently widely used to treat hypertension, is Bisoprolol.
Beta blockers: side effects
- decrease in heart rate;
- slowing of atrioventricular conduction;
- a significant decrease in blood pressure;
- reduction of ejection fraction.
- disorders of the respiratory system (bronchospasm, violation of bronchial obstruction, exacerbation of chronic lung diseases);
- peripheral vasoconstriction (Raynaud’s syndrome, cold extremities, intermittent claudication);
- psycho-emotional disorders (weakness, drowsiness, memory impairment, emotional lability, depression, acute psychoses, sleep disturbances, hallucinations);
- gastrointestinal disorders (nausea, diarrhea, abdominal pain, constipation, exacerbation of peptic ulcer, colitis);
- withdrawal syndrome;
- violation of carbohydrate and lipid metabolism;
- muscle weakness, intolerance to physical exertion;
- impotence and decreased libido;
- decreased renal function due to decreased perfusion;
- decreased production of tear fluid, conjunctivitis;
- skin disorders (dermatitis, exanthema, exacerbation of psoriasis);
- fetal malnutrition.
Which beta blocker is better?
Speaking of beta-blockers as a class of antihypertensive drugs, they mean drugs with beta-1 selectivity (have fewer side effects), without internal sympathomimetic activity (more effective) and vasodilating properties.
More recently, a beta-blocker has appeared in our country, which has the most optimal combination of all the qualities necessary for the treatment of chronic diseases (arterial hypertension and coronary heart disease) – Lokren.
Lokren is an original and at the same time inexpensive beta-blocker, which has high beta-1 selectivity and the longest half-life (15-20 hours), which allows it to be used once a day. However, he does not have an internal sympathomimetic activity. The drug normalizes the variability of the daily rhythm of blood pressure, helps to reduce the degree of morning increase in blood pressure.
The second drug that can be distinguished is Nebilet (Nebivolol). It occupies a special place in the class of beta-blockers because of its unusual properties. A non-ticket consists of two isomers: the first of them is a beta blocker, and the second is a vasodilator. The drug has a direct effect on the stimulation of the synthesis of nitric oxide (NO) by vascular endothelium.
Due to the double mechanism of action, Nebilet can be prescribed to a patient with arterial hypertension and concomitant chronic obstructive pulmonary diseases, peripheral arterial atherosclerosis, congestive heart failure, severe dyslipidemia and diabetes mellitus.
As for the last two pathological processes, today there is a significant amount of scientific evidence that Nebilet not only does not adversely affect lipid and carbohydrate metabolism, but also normalizes the effect on cholesterol, triglycerides, blood glucose and glycated hemoglobin. Researchers associate these properties, unique to the class of beta-blockers, with the NO-modulating activity of the drug.
Medications containing β-blockers are prohibited in the following pathologies:
- acute heart failure;
- low blood pressure
- individual intolerance to the components of the drug;
- short syndrome.
Alpha-blocker-based medications are not used by patients with features such as:
- the period of pregnancy and lactation in women;
- severe liver and kidney dysfunction;
- low blood pressure;
- the presence of severe heart disease;
- individual intolerance to the components.
Beta blocker withdrawal syndrome
The sudden cancellation of beta-adrenoreceptor blockers after their prolonged use, especially in high doses, can cause phenomena characteristic of the clinical picture of unstable angina, ventricular tachycardia, myocardial infarction, and sometimes lead to sudden death. Withdrawal syndrome begins to appear a few days later (less often – 2 weeks) after stopping beta-adrenergic blockers.
To prevent the serious consequences of the withdrawal of these drugs, you must adhere to the following recommendations:
- stop using beta-adrenoreceptor blockers gradually, over 2 weeks, according to this scheme: on the 1st day, the daily dose of propranolol is reduced by no more than 80 mg, on the 5th – by 40 mg, on the 9th – by 20 mg and on the 13th – 10 mg;
- patients with coronary heart disease during and after the withdrawal of beta-adrenergic blockers should limit physical activity and, if necessary, increase the dose of nitrates;
- beta-adrenergic blockers are not canceled before surgery for patients with coronary artery disease who are scheduled for coronary artery bypass grafting, 2 hours before surgery, 1/2 daily dose is prescribed, no beta-blockers are administered during surgery, but within 2 days. after it is prescribed intravenously.
Detonic – a unique medicine that helps fight hypertension at all stages of its development.
The complex effect of plant components of the drug Detonic on the walls of blood vessels and the autonomic nervous system contribute to a rapid decrease in blood pressure. In addition, this drug prevents the development of atherosclerosis, thanks to the unique components that are involved in the synthesis of lecithin, an amino acid that regulates cholesterol metabolism and prevents the formation of atherosclerotic plaques.
Detonic not addictive and withdrawal syndrome, since all components of the product are natural.
Detailed information about Detonic is located on the manufacturer’s page.