These drugs share a number of characteristics with ACE inhibitors. Their effect on mortality and life expectancy is actively studied in numerous clinical studies, which end in 4-6 years. AT 1 -receptor blockers are indicated for intolerance to ACE inhibitors and are contraindicated in pregnancy, bilateral renal artery stenosis, hyperkalemia.

ACE inhibitors do not completely block the formation of A-II, since the production of this hormone is also controlled by tissue plasminogen activator, cathepsin G, chymase, and this pathway of A-II formation in pathological conditions is the leading one.

By chemical structure, AT 1 receptor blockers are derivatives of the following compounds:

Biphenyltetrazolics (losartan);

Nebiphenyltetrazolics (Eposartan, Telmisartan);

Non-heterocyclic (valsartan).

Losartan (kosaar), irbesartan (aprovel), candesartan (atakand), telmisartan (priitor, micardis), eprosartan (teveten).

Losartanappoint 50-100 mg once a day, with high doses of diuretics and with impaired liver and kidney function, the initial dose is reduced to 25 mg / day.

-blockers

Safely and effectively lower blood pressure, are the means of choice for BPH and uterine fibroids. Possible indications for their appointment are considered impaired glucose tolerance and dyslipidemia. Orthostatic hypotension is a relative contraindication; therefore, in elderly patients, -AB should be used with caution under control of blood pressure in a standing position.

In February 2000, the safety committee discontinued the use of doxazazin in the ALLHAT study due to a significantly higher incidence of congestive heart failure compared with other treatment regimens.

There are 2 main groups:

 1 -AB: prazosin, doxazosin, terazosin;

 1  2 -AB: ketanserin, indoramine.

Doxazosin(kardura). Blood pressure decreases gradually, the maximum effect is observed after 2-6 hours and lasts 24 hours. The dose ranges from 1 to 16 mg / day. Treatment should be started with a dose of 1 mg once a day for 1-2 weeks, then in the next 1-2 weeks the dose should be increased to 2 mg / day. To achieve the desired effect, the daily dose should be increased gradually, observing uniform intervals, up to 4, 8 and 16 mg, depending on the severity of the patient's response. The usual dose is 2-4 mg once a day.

Phentolamine(dibazin) - available in a solution for intravenous administration of 5 mg of phentolamine together with 25 mg of mannitol in one ampoule, as well as in tablets of 0.02 g. The onset of the effect occurs immediately, the peak of the effect is 2-5 minutes after intravenous administration, duration action 5-10 minutes. It is indicated for hypertensive crises with pheochromocytoma. In case of crises, it is administered intravenously in the form of a bolus of 5-20 mg, then an intravenous infusion of 100-500 mg / l at a rate of 0.5-1 mg / min is possible, or re-administration of a bolus after 1-2 hours.

Selective agonists of j1 receptors (imidazoline)

J 1 receptors are located in the rostral ventrolateral part of the medulla oblongata, are responsible for tonic and reflex control of the sympathetic nervous system. Activation of these receptors leads to inhibition of interneurons of the intermediate zone of the SM, which causes the suppression of sympathetic preganglionic neurons of the SM. This is accompanied by inhibition of SNS activity with a subsequent decrease in the release of CA.

Stimulation of peripheral imidazoline receptors affects metabolic homeostasis: an increase in glucose-dependent insulin release and glucose transport into cells, followed by a decrease in glycemia, an increase in aerobic glucose oxidation and glycogen synthesis, a decrease in lactate production, and an increase in brain tissue glucose sensitivity.

Moxonidine(zint, physiotens) in EH is used in an initial dose of 0.2 mg once a day, later, if necessary, the dose can be increased to 0.4-0.6 mg once a day. Contraindications:

AV block II-III degree;

Severe arrhythmias;

Bradycardia less than 50 per minute;

Severe heart failure;

Unstable angina;

Hepatic and renal failure;

Indications of Quincke's edema in anamnesis.

With metabolic syndrome, the use of a combination of an ACE inhibitor and zinc is justified.

Angiotensin receptor blockers (AT 1 receptor blockers)

According to the mechanism of action, blockers of angiotensin receptors (BAR), like ACE inhibitors, affect the renin-angiotensin system. However, this class works "more targeted", as it removes the excessive effects of angiotensin and aldosterone by blocking AT receptors, which these pressor (BP increasing) agents act on. BAR prevents the formation of angiotensin, a substance that causes vasoconstriction and vasodilation. As a result, blood pressure decreases.

Currently in the arsenal of doctors there are a number of representatives of this group. The most widely used was the first representative of this group - losartan. The action of all drugs in this group is comparable in effectiveness and duration (up to 24 hours). Telmisartan has the longest effect (up to 36 hours), allowing long-term control of blood pressure. This drug has a number of other features, since it has a positive effect on carbohydrate metabolism, and it should be given preference in diabetes mellitus. It is indicated for patients with kidney disease.

Have you taken AT1 receptor blockers, ACE inhibitors before, how did you react to them, did you bother with a dry cough.

Have you been diagnosed with changes in the kidneys, liver.

You are pregnant or want to have a baby in the near future, what kind of contraception are you using.

Subgroup preparations excluded... Enable

Description

Angiotensin II receptor antagonists, or AT 1 receptor blockers, are one of the new groups of antihypertensive drugs. It combines drugs that modulate the functioning of the renin-angiotensin-aldosterone system (RAAS) through interaction with angiotensin receptors.

RAAS plays an important role in the regulation of blood pressure, the pathogenesis of arterial hypertension and chronic heart failure (CHF), as well as a number of other diseases. Angiotensins (from angio - vascular and tensio - tension) - peptides formed in the body from angiotensinogen, which is a glycoprotein (alpha 2 -globulin) of blood plasma, synthesized in the liver. Under the influence of renin (an enzyme formed in the juxtaglomerular apparatus of the kidneys), the angiotensinogen polypeptide, which does not possess pressor activity, is hydrolyzed, forming angiotensin I, a biologically inactive decapeptide that is easily subject to further transformations. Under the action of angiotensin-converting enzyme (ACE), which is formed in the lungs, angiotensin I is converted into an octapeptide - angiotensin II, which is a highly active endogenous pressor compound.

Angiotensin II is the main effector peptide of the RAAS. It has a strong vasoconstrictor effect, increases OPSS, causes a rapid increase in blood pressure. In addition, it stimulates the secretion of aldosterone, and in high concentrations, it increases the secretion of antidiuretic hormone (increased sodium and water reabsorption, hypervolemia) and causes sympathetic activation. All these effects contribute to the development of hypertension.

Angiotensin II is rapidly metabolized (half-life - 12 min) with the participation of aminopeptidase A to form angiotensin III and then under the influence of aminopeptidase N - angiotensin IV, which have biological activity. Angiotensin III stimulates the production of aldosterone by the adrenal glands, has a positive inotropic activity. Angiotensin IV is presumably involved in the regulation of hemostasis.

It is known that in addition to the RAAS of systemic blood flow, the activation of which leads to short-term effects (including such as vasoconstriction, increased blood pressure, secretion of aldosterone), there are local (tissue) RAAS in various organs and tissues, incl. in the heart, kidneys, brain, blood vessels. The increased activity of tissue RAAS determines the long-term effects of angiotensin II, which are manifested by structural and functional changes in target organs and lead to the development of such pathological processes as myocardial hypertrophy, myofibrosis, atherosclerotic lesions of cerebral vessels, kidney damage, etc.

It has now been shown that in humans, in addition to the ACE-dependent pathway for converting angiotensin I to angiotensin II, there are alternative pathways involving chymases, cathepsin G, tonin, and other serine proteases. Chymases, or chymotrypsin-like proteases, are glycoproteins with a molecular weight of about 30,000. Chymases have a high specificity for angiotensin I. In different organs and tissues, either ACE-dependent or alternative pathways of angiotensin II formation prevail. Thus, in the tissue of the human myocardium, cardiac serine protease, its DNA and mRNA were found. Moreover, the largest amount of this enzyme is contained in the left ventricular myocardium, where the chymase pathway accounts for more than 80%. Chemase-dependent formation of angiotensin II prevails in the myocardial interstitium, adventitia, and vascular media, while ACE-dependent formation prevails in blood plasma.

Angiotensin II can also be formed directly from angiotensinogen by reactions catalyzed by tissue plasminogen activator, tonin, cathepsin G, etc.

It is believed that the activation of alternative pathways for the formation of angiotensin II plays an important role in the processes of cardiovascular remodeling.

The physiological effects of angiotensin II, like other biologically active angiotensins, are realized at the cellular level through specific angiotensin receptors.

To date, the existence of several subtypes of angiotensin receptors has been established: AT 1, AT 2, AT 3 and AT 4, etc.

In humans, two subtypes of membrane-bound, G-protein coupled angiotensin II receptors have been identified and most fully studied - subtypes AT 1 and AT 2.

AT 1 receptors are localized in various organs and tissues, mainly in the smooth muscles of blood vessels, heart, liver, adrenal cortex, kidneys, lungs, in some areas of the brain.

Most of the physiological effects of angiotensin II, including the unfavorable ones, are mediated by AT 1 receptors:

Arterial vasoconstriction, incl. vasoconstriction of the arterioles of the renal glomeruli (especially the efferent), increased hydraulic pressure in the renal glomeruli,

Enhanced sodium reabsorption in the proximal renal tubules,

Secretion of aldosterone by the adrenal cortex,

Secretion of vasopressin, endothelin-1,

Renin release

Increased release of norepinephrine from sympathetic nerve endings, activation of the sympathetic-adrenal system,

Proliferation of vascular smooth muscle cells, intimal hyperplasia, cardiomyocyte hypertrophy, stimulation of vascular and heart remodeling processes.

In arterial hypertension against the background of excessive activation of the RAAS, the effects of angiotensin II mediated by AT 1 receptors directly or indirectly contribute to an increase in blood pressure. In addition, the stimulation of these receptors is accompanied by the damaging effect of angiotensin II on the cardiovascular system, including the development of myocardial hypertrophy, thickening of the arterial walls, etc.

The effects of angiotensin II mediated by AT 2 receptors have been discovered only in recent years.

A large number of AT 2 receptors have been found in fetal tissues (including the brain). In the postnatal period, the number of AT 2 receptors in human tissues decreases. Experimental studies, in particular in mice in which the gene encoding AT 2 receptors was disrupted, suggest their participation in growth and maturation processes, including cell proliferation and differentiation, development of embryonic tissues, and the formation of exploratory behavior.

AT 2 receptors are found in the heart, blood vessels, adrenal glands, kidneys, some areas of the brain, reproductive organs, incl. in the uterus, atresized ovarian follicles, as well as in skin wounds. It has been shown that the number of AT 2 -receptors can increase with tissue damage (including vessels), myocardial infarction, heart failure. It is assumed that these receptors may be involved in the processes of tissue regeneration and programmed cell death (apoptosis).

Recent studies show that the cardiovascular effects of angiotensin II mediated by AT 2 receptors are opposite to the effects caused by the excitation of AT 1 receptors and are relatively weak. Stimulation of AT 2 receptors is accompanied by vasodilation, inhibition of cell growth, incl. suppression of cell proliferation (endothelial and smooth muscle cells of the vascular wall, fibroblasts, etc.), inhibition of cardiomyocyte hypertrophy.

The physiological role of type II angiotensin II receptors (AT 2) in humans and their relationship with cardiovascular homeostasis is currently not fully understood.

Highly selective antagonists of AT 2 receptors (CGP 42112A, PD 123177, PD 123319), which are used in experimental studies of the RAAS, have been synthesized.

Other angiotensin receptors and their role in humans and animals are poorly understood.

The subtypes of AT 1 receptors - AT 1a and AT 1b, differing in affinity for peptide agonists of angiotensin II (these subtypes were not found in humans) were isolated from the rat mesangium cell culture. The AT 1c receptor subtype was isolated from the rat placenta, the physiological role of which is not yet clear.

AT 3 receptors with an affinity for angiotensin II are found on the membranes of neurons, their function is unknown. AT 4 receptors are found on endothelial cells. By interacting with these receptors, angiotensin IV stimulates the release of type 1 plasminogen activator inhibitor from the endothelium. AT 4 receptors are also found on the membranes of neurons, incl. in the hypothalamus, presumably in the brain, they mediate cognitive functions. In addition to angiotensin IV, angiotensin III also possesses tropism for AT 4 receptors.

Long-term studies of the RAAS not only revealed the importance of this system in the regulation of homeostasis, in the development of cardiovascular pathology, the effect on the functions of target organs, among which the most important are the heart, blood vessels, kidneys and brain, but also led to the creation of medicines, purposefully acting on individual links of the RAAS.

The scientific basis for the creation of drugs that act by blocking angiotensin receptors was the study of angiotensin II inhibitors. Experimental studies show that angiotensin II antagonists capable of blocking its formation or action and thus reducing the activity of the RAAS are inhibitors of the formation of angiotensinogen, inhibitors of renin synthesis, inhibitors of the formation or activity of ACE, antibodies, antagonists of angiotensin receptors, including synthetic, non-peptide compounds specifically blocking AT 1 receptors, etc.

The first blocker of angiotensin II receptors, introduced into therapeutic practice in 1971, was saralazin, a peptide compound similar in structure to angiotensin II. Saralazin blocked the pressor action of angiotensin II and lowered the tone of peripheral vessels, decreased the plasma aldosterone content, and lowered blood pressure. However, by the mid-70s, the experience of using saralazine showed that it has the properties of a partial agonist and in some cases gives a poorly predictable effect (in the form of excessive hypotension or hypertension). At the same time, a good hypotensive effect was manifested in conditions associated with a high level of renin, while against the background of a low level of angiotensin II or with a rapid injection of blood pressure increased. Due to the presence of agonistic properties, as well as due to the complexity of the synthesis and the need for parenteral administration, saralazine has not received wide practical use.

In the early 90s, the first non-peptide selective antagonist of AT 1 -receptors, effective when taken orally, losartan, was synthesized, which has received practical application as an antihypertensive agent.

Currently, in the world medical practice, several synthetic non-peptide selective AT 1 -blockers are used or are undergoing clinical trials - valsartan, irbesartan, candesartan, losartan, telmisartan, eprosartan, olmesartan medoxomil, azilsartan medoxomil, zolarsartan and pokazolarsartan, tazosartan Russia).

There are several classifications of angiotensin II receptor antagonists: by chemical structure, pharmacokinetic characteristics, mechanism of binding to receptors, etc.

According to their chemical structure, non-peptide AT 1 receptor blockers can be divided into 3 main groups:

Biphenyl derivatives of tetrazole: losartan, irbesartan, candesartan, valsartan, tazosartan;

Biphenyl non-tetrazole compounds - telmisartan;

Non-phenyl non-tetrazole compounds - eprosartan.

By the presence of pharmacological activity, AT 1 -receptor blockers are divided into active dosage forms and prodrugs. So, valsartan, irbesartan, telmisartan, eprosartan themselves have pharmacological activity, while candesartan cilexetil becomes active only after metabolic transformations in the liver.

In addition, AT 1 -blockers differ depending on the presence or absence of active metabolites. Active metabolites are found in losartan and tazosartan. For example, the active metabolite of losartan, EXP-3174, has a stronger and longer-lasting effect than losartan (in terms of pharmacological activity, EXP-3174 is 10-40 times higher than losartan).

By the mechanism of binding to receptors, AT 1 receptor blockers (as well as their active metabolites) are divided into competitive and non-competitive angiotensin II antagonists. Thus, losartan and eprosartan bind reversibly to AT 1 receptors and are competitive antagonists (i.e., under certain conditions, for example, with an increase in the level of angiotensin II in response to a decrease in BCC, they can be displaced from the binding sites), while valsartan, irbesartan , candesartan, telmisartan, as well as the active metabolite of losartan EXP-3174, act as noncompetitive antagonists and bind irreversibly to receptors.

The pharmacological action of the drugs in this group is due to the elimination of the cardiovascular effects of angiotensin II, incl. vasopressor.

It is believed that the antihypertensive effect and other pharmacological effects of angiotensin II receptor antagonists are realized in several ways (one direct and several indirect).

The main mechanism of action of drugs in this group is associated with the blockade of AT 1 receptors. All of them are highly selective AT 1 receptor antagonists. It has been shown that their affinity for AT 1 exceeds that for AT 2 receptors by a factor of 1000: for losartan and eprosartan by more than 1 thousand times, telmisartan - more than 3 thousand, irbesartan - 8.5 thousand, active metabolite of losartan EXP-3174 and candesartan - 10 thousand times, olmesartan - 12.5 thousand times, valsartan - 20 thousand times.

The blockade of AT 1 receptors prevents the development of the effects of angiotensin II, mediated by these receptors, which prevents the adverse effect of angiotensin II on vascular tone and is accompanied by a decrease in elevated blood pressure. Long-term use of these drugs leads to a weakening of the proliferative effects of angiotensin II on vascular smooth muscle cells, mesangial cells, fibroblasts, a decrease in cardiomyocyte hypertrophy, etc.

It is known that AT 1 -receptors of cells of the juxtaglomerular apparatus of the kidneys are involved in the process of regulation of renin release (according to the principle of negative feedback). The blockade of AT 1 receptors causes a compensatory increase in renin activity, an increase in the production of angiotensin I, angiotensin II, etc.

In conditions of an increased content of angiotensin II against the background of blockade of AT 1 receptors, the protective properties of this peptide are manifested, which are realized through stimulation of AT 2 receptors and are expressed in vasodilation, slowing down of proliferative processes, etc.

In addition, against the background of an increased level of angiotensins I and II, the formation of angiotensin- (1-7) occurs. Angiotensin- (1-7) is formed from angiotensin I under the action of neutral endopeptidase and from angiotensin II under the action of prolyl endopeptidase and is another effector peptide of the RAAS that has vasodilating and natriuretic effects. The effects of angiotensin- (1-7) are mediated through the so-called, not yet identified, AT x receptors.

Recent studies of endothelial dysfunction in hypertension suggest that the cardiovascular effects of angiotensin receptor blockers may also be associated with endothelial modulation and effects on nitric oxide (NO) production. The experimental data obtained and the results of individual clinical studies are rather contradictory. Perhaps, against the background of blockade of AT 1 receptors, endothelium-dependent synthesis and release of nitric oxide increases, which contributes to vasodilation, a decrease in platelet aggregation and a decrease in cell proliferation.

Thus, the specific blockade of AT 1 receptors provides a pronounced antihypertensive and organoprotective effect. Against the background of blockade of AT 1 receptors, the adverse effect of angiotensin II (and angiotensin III, which has an affinity for angiotensin II receptors) on the cardiovascular system is inhibited and, presumably, its protective effect is manifested (by stimulating AT 2 receptors), and the action also develops angiotensin- (1-7) by stimulation of AT x -receptors. All these effects contribute to vasodilation and weakening of the proliferative action of angiotensin II in relation to vascular and heart cells.

AT 1 -receptor antagonists can penetrate the blood-brain barrier and inhibit the activity of mediator processes in the sympathetic nervous system. By blocking the presynaptic AT 1 receptors of sympathetic neurons in the central nervous system, they inhibit the release of norepinephrine and reduce the stimulation of vascular smooth muscle adrenergic receptors, which leads to vasodilation. Experimental studies show that this additional mechanism of vasodilatory action is more characteristic of eprosartan. Data on the effect of losartan, irbesartan, valsartan, etc. on the sympathetic nervous system (which manifested itself at doses exceeding therapeutic ones) are very contradictory.

All AT 1 receptor blockers act gradually, the antihypertensive effect develops smoothly, within several hours after taking a single dose, and lasts up to 24 hours. With regular use, a pronounced therapeutic effect is usually achieved after 2-4 weeks (up to 6 weeks) of treatment.

Features of the pharmacokinetics of this group of drugs make their use by patients convenient. These medicines can be taken with or without food. A single dose is enough to provide a good hypotensive effect during the day. They are equally effective in patients of different sex and age, including patients over 65 years of age.

Clinical studies show that all angiotensin receptor blockers have a high antihypertensive and pronounced organoprotective effect, good tolerance. This allows them to be used, along with other antihypertensive drugs, for the treatment of patients with cardiovascular pathology.

The main indication for the clinical use of angiotensin II receptor blockers is the treatment of arterial hypertension of varying severity. Possible monotherapy (with mild arterial hypertension) or in combination with other antihypertensive drugs (with moderate and severe forms).

Currently, according to the recommendations of the WHO / IOG (International Society for Hypertension), preference is given to combination therapy. The most rational for angiotensin II receptor antagonists is their combination with thiazide diuretics. The addition of a diuretic at low doses (eg, 12.5 mg hydrochlorothiazide) can improve the effectiveness of therapy, as evidenced by the results of randomized multicenter trials. Preparations have been created that include this combination - Gizaar (losartan + hydrochlorothiazide), Co-diovan (valsartan + hydrochlorothiazide), Coaprovel (irbesartan + hydrochlorothiazide), Atakand Plus (candesartan + hydrochlorothiazide) (telicardis + hydrochlorothiazide), Micardis Plus ...

A number of multicenter studies (ELITE, ELITE II, Val-HeFT, etc.) have shown the efficacy of using some AT 1 receptor antagonists in CHF. The results of these studies are ambiguous, but in general they indicate a high efficacy and better (compared to ACE inhibitors) tolerance.

The results of experimental and clinical studies indicate that blockers of AT 1 -subtype receptors not only prevent the processes of cardiovascular remodeling, but also cause the reverse development of left ventricular hypertrophy (LVH). In particular, it was shown that with long-term therapy with losartan, patients showed a tendency to a decrease in the size of the left ventricle during systole and diastole, an increase in myocardial contractility. Regression of LVH was observed with long-term use of valsartan and eprosartan in patients with arterial hypertension. Some receptor blockers of the AT 1 subtype have been found to improve renal function, incl. with diabetic nephropathy, as well as indicators of central hemodynamics in CHF. While clinical observations regarding the effect of these drugs on target organs are few, but research in this area is actively continuing.

Contraindications to the use of blockers of angiotensin AT 1 receptors are individual hypersensitivity, pregnancy, breastfeeding.

The data obtained in experiments on animals indicate that agents that have a direct effect on the RAAS can cause damage to the fetus, the death of the fetus and the newborn. Especially dangerous is the effect on the fetus in the II and III trimesters of pregnancy, because possible development of hypotension, hypoplasia of the skull, anuria, renal failure and death in the fetus. There are no direct indications of the development of such defects when taking AT 1 receptor blockers, however, the drugs of this group should not be used during pregnancy, and if pregnancy is detected during the treatment period, they should be discontinued.

There is no information on the ability of AT 1 receptor blockers to penetrate into the breast milk of women. However, in experiments on animals, it was found that they penetrate into the milk of lactating rats (significant concentrations of not only the substances themselves, but also their active metabolites are found in the milk of rats). In this regard, AT 1 receptor blockers are not used in lactating women, and if therapy is necessary for the mother, breastfeeding is stopped.

You should refrain from using these drugs in pediatric practice, since the safety and effectiveness of their use in children have not been determined.

There are several limitations for therapy with AT 1 antagonists of angiotensin receptors. Caution should be exercised in patients with reduced BCC and / or hyponatremia (during treatment with diuretics, restriction of salt intake with diet, diarrhea, vomiting), as well as in patients on hemodialysis, because development of symptomatic hypotension is possible. Assessment of the risk / benefit ratio is necessary in patients with renovascular hypertension due to bilateral renal artery stenosis or renal artery stenosis of a solitary kidney. excessive inhibition of the RAAS in these cases increases the risk of severe hypotension and renal failure. It should be used with caution in aortic or mitral stenosis, obstructive hypertrophic cardiomyopathy. With impaired renal function, monitoring of serum potassium and creatinine levels is necessary. Not recommended for patients with primary hyperaldosteronism, because in this case, drugs that inhibit the RAAS are ineffective. There are insufficient data on the use in patients with severe liver disease (for example, with cirrhosis).

Hitherto reported side effects with angiotensin II receptor antagonists are usually mild, transient, and rarely warrant discontinuation of therapy. The overall incidence of side effects is comparable to placebo, as evidenced by the results of placebo-controlled studies. The most common adverse effects are headache, dizziness, general weakness, etc. Angiotensin receptor antagonists do not directly affect the metabolism of bradykinin, substance P, and other peptides and, as a result, do not cause dry cough, which often occurs during treatment with ACE inhibitors.

When taking drugs of this group, there is no effect of hypotension of the first dose, which occurs when taking ACE inhibitors, and sudden cancellation is not accompanied by the development of rebound hypertension.

The results of multicenter, placebo-controlled studies show high efficacy and good tolerance of AT 1 -receptor angiotensin II antagonists. However, while their use is limited by the lack of data on the long-term effects of their use. According to WHO / MTF experts, their use for the treatment of arterial hypertension is advisable in case of intolerance to ACE inhibitors, in particular, in case of indication of a history of cough caused by ACE inhibitors.

Numerous clinical studies are ongoing, incl. and multicenter, devoted to the study of the efficacy and safety of the use of angiotensin II receptor antagonists, their effect on mortality, duration and quality of life of patients and in comparison with antihypertensive and other drugs in the treatment of arterial hypertension, chronic heart failure, atherosclerosis, etc.

Drugs

Preparations - 4133 ; Trade names - 84 ; Active ingredients - 9

How to live without a heart attack and stroke Anton Vladimirovich Rodionov

Angiotensin receptor blockers (AT1 receptor blockers)

How do AT 1 receptor blockers work?

The mechanism of action of angiotensin receptor blockers is very similar to ACE inhibitors. They prevent the formation of a substance that causes vasoconstriction, and the vessels dilate. As a result, blood pressure decreases.

What are AT 1 receptor blockers?

AT 1 receptor blockers are the youngest group of drugs, although they have been used for about 20 years. Currently, there are 7 representatives of this group in the arsenal of doctors. The most widely used was the first representative of this group - losartan ( kosaar, lozap, lorista). All drugs, except for losartan, can be taken once a day, losartan is usually taken 2 times a day. The only drawback of AT 1 receptor blockers is their high cost.

Losartan (kosaar)- take 1-2 times a day

Valsartan (diovan, valz, valsacor)- take once a day

Irbesartan (april)- take once a day

Candesartan (atacand)- take once a day

Telmisartan (micardis)- take once a day

Eprosartan (teveten)- take once a day

Olmesartan ( cardosal)- take once a day

Why are AT 1 receptor blockers good?

AT 1 receptor blockers have the advantages of ACE inhibitors and are significantly less likely to cause side effects.

Angiotensin receptor blockers are a relatively new group of drugs, but over the past 10 years there has been good evidence that they can reduce the risk of cardiovascular complications, including in patients with diabetes mellitus and heart failure.

In what cases does the doctor prescribe AT 1 receptor blockers?

AT 1 -receptor blockers are used in the same cases as ACE inhibitors. Angiotensin receptor blockers are more often used when ACE inhibitors have a sufficient effect, but cause severe side effects (in particular, cough).

When should you not prescribe AT 1 receptor blockers?

AT 1 receptor blockers should not be taken by pregnant women. They should not be taken with an increased potassium content in the blood (hyperkalemia), narrowing (stenosis) of the renal arteries.

Be sure to tell your doctor:

Have you taken AT 1 - receptor blockers, ACE inhibitors before, how did you react to them, did you bother with a dry cough.

Have you been diagnosed with changes in the kidneys, liver.

You are pregnant or want to have a baby in the near future, what kind of contraception are you using.

How should I take AT 1 receptor blockers?

The drugs of this group are taken once a day at the same time. It should be borne in mind that the effect (ie, a steady decrease in blood pressure) does not occur immediately, but only after 2-4 weeks of continuous treatment.

What side reactions are possible with the use of AT 1 receptor blockers?

Drugs in this group are usually well tolerated. In the majority of patients, there were no adverse reactions when taking AT 1 receptor blockers. In some cases, dizziness, hives, and itching may occur.