Analysis of the effectiveness and safety of moxonidine in patients with arterial hypertension and hypertensive crises

Moxonidine

Moxonidine is an antihypertensive drug belonging to the group of selective imidazoline receptor agonists. Arterial hypertension is the most common disease in our country. This can be judged at least by the steadily increasing frequency of ambulance calls during hypertensive crises. In this regard, adequate pharmacotherapy becomes more important than ever. Unfortunately, some antihypertensive drugs, while effectively lowering blood pressure, can cause adverse metabolic effects, which somewhat narrows the prospects for their further use. An example is beta-blockers, which, along with successfully reducing excessive activity, hyperactivity of the sympathetic nervous system can contribute to the occurrence of hypoglycemia in people with diabetes. In addition to this fly in the ointment, taking beta-blockers can provoke bronchospasm and worsen the prognosis in patients with bronchial asthma and chronic obstructive pulmonary disease. Due to the large role of sympathetic hyperactivity in the development of arterial hypertension, a new generation of symptatolytics, one of which is moxonidine, has recently been increasingly introduced into cardiological practice. Sympatholytics reduce blood pressure by selectively acting on the vasomotor centers of the medulla oblongata, which regulate the tone of the sympathetic nervous system. The “pioneers” of this pharmacological group were clonidine and methyldopa, and later second-generation drugs appeared, including moxonidine. Unlike first generation sympatholytics, it has a low degree of affinity for alpha-2 adrenergic receptors localized in the brain stem, which significantly reduces the risk of side effects, including dry mouth and sedation. The selectivity of the drug for I1-imidazoline receptors is more than 70 times greater than that for alpha2-adrenergic receptors.

At recommended doses, moxonidine is devoid of clinically significant side effects and causes a dose-dependent decrease in blood pressure, while the heart rate remains virtually unchanged. After discontinuation of moxonidine, the development of withdrawal syndrome is uncharacteristic. The drug reduces the concentration of renin, angiotensin II and aldosterone in the blood, which is of particular importance for the prevention of the development and progression of pathological changes in the heart and blood vessels. Relief of sympathetic hyperactivity under the influence of moxonidine is accompanied by a decrease in tissue insulin resistance and normalization of carbohydrate and lipid metabolism. In this regard, moxonidine is rightfully considered the drug of choice for the treatment of arterial hypertension in diabetics and people with metabolic syndrome. According to clinical trials, the antihypertensive activity of the drug is quite comparable to that of beta-blockers, diuretics, slow calcium channel blockers and ACE inhibitors. Moxonidine acts in two directions: on the cerebral sympathetic centers (short-term blood pressure control) and on renin release and renal excretory function (long-term blood pressure control). The drug has another interesting feature: it is more effective in patients with initially higher blood pressure levels. Therefore, the prospect of its use in hypertensive crises is of particular interest. A positive effect of moxonidine on the course of arterial hypertension in patients with chronic obstructive pulmonary disease was also revealed. Thus, moxonidine is a universal antihypertensive drug that is effective both in hypertensive crises and over a longer “distance”.

Centrally acting drug moxonidine in the treatment of arterial hypertension

According to epidemiological studies, the prevalence of arterial hypertension (AH) among adults in developed countries ranges from 20% to 40% and increases with age [3]. Elevated blood pressure is found in more than 50% of men and women over 60 years of age [4]. The relevance of the problem is supported by the increasing processes of urbanization of society, which create the preconditions for the emergence of risk factors such as stress, physical inactivity, obesity, bad habits and disturbed ecology. High blood pressure is one of the main risk factors for the development of cerebral stroke, coronary heart disease (CHD) and other cardiovascular diseases of atherosclerotic origin, which are associated with more than 50% of all deaths [5]. According to modern national recommendations [6], recommendations of the European Society of Arterial Hypertension and the European Society of Cardiology [7], the treatment tactics for essential hypertension depend on the level of blood pressure and the degree of risk of cardiovascular complications. The main goal of treatment is to minimize the risk of developing cardiovascular complications and death from them. The main objectives are normalization of blood pressure levels in order to prevent complications in the absence or minimal level of adverse drug reactions, correction of all modifiable risk factors (smoking, dyslipidemia, hyperglycemia, obesity), prevention, slowing down the rate of progression and/or reducing target organ damage, as well as treatment of associated and concomitant diseases - ischemic heart disease, diabetes mellitus (DM), etc. [6, 7]. When treating patients with hypertension, blood pressure should be less than 140/90 mm Hg. Art., which is its target level. If the prescribed therapy is well tolerated, it is advisable to reduce blood pressure to lower values. In patients with a high and very high risk of cardiovascular complications, it is necessary to reduce blood pressure to 140/90 mmHg. Art. or less within 4 weeks. In the future, subject to good tolerance, it is recommended to reduce blood pressure to 130/80 mmHg. Art. and less. In patients with coronary artery disease, blood pressure should be reduced to the target value of 130/85 mm Hg. Art. In patients with diabetes and/or kidney disease, the target blood pressure level should be less than 130/85 mmHg. Art. [6]. There are no uniform recommendations regarding which drugs should be used to start treating a patient. The choice of drug depends on many factors, including age, gender and the presence of concomitant diseases. Currently, 5 main classes of antihypertensive drugs are recommended for the treatment of hypertension: angiotensin-converting enzyme inhibitors (ACEIs), AT1 receptor blockers (ARBs), calcium antagonists (CAs), β-blockers (BABs), and diuretics. α-blockers, imidazoline I1 receptor agonists, and direct renin inhibitors can be used as additional classes for combination antihypertensive therapy [6, 7].

Agonists of imidazoline receptors (moxonidine, rilmenidine) are modern drugs with a central mechanism of action - they reduce the activity of the vasomotor center of the medulla oblongata. Centrally acting antihypertensive drugs also include clonidine, guanfacine, and methyldopa [1, 2]. Moxonidine (Moxarel, JSC "Vertex", Russia) is a highly selective agonist of imidazoline I1 receptors located in the rostral ventrolateral part of the medulla oblongata. Stimulation of these receptors reduces sympathetic flow and, accordingly, blood pressure by reducing vascular resistance. In addition, the activity of the vasomotor center decreases, cardiac output and peripheral sympathetic activity decrease. Taking moxonidine leads to a decrease in systemic vascular resistance and blood pressure. Moxonidine reduces the levels of renin, angiotensin II and aldosterone in the blood plasma [20]. After oral administration, the peak concentration is reached within 1 hour. The half-life in plasma is 2 hours and increases with renal failure. Despite the relatively short half-life, blood pressure is effectively regulated with a single dose of the drug per day. The antihypertensive effect lasts much longer, which is due to the retention of the drug in the central nervous system. The sympathoinhibitory effect of moxonidine is probably mediated almost entirely by its effect on I receptors. Moxonidine differs from other sympatholytic antihypertensive drugs in its lower affinity for central α2-adrenergic receptors, which explains the lower likelihood of developing sedation and dry mouth compared to clonidine. The antihypertensive effectiveness of moxonidine in essential hypertension has been proven in large-scale, double-blind, placebo-controlled, randomized studies and is comparable to that of most other antihypertensive drugs [8].

Food intake does not affect the pharmacokinetics of the drug. The drug is well absorbed from the gastrointestinal tract and is almost completely absorbed in its upper sections. Absolute bioavailability is approximately 88%. The maximum concentration in the blood is recorded after 0.5–3 hours. The connection with blood plasma proteins is 7.2%. 90% of the drug is excreted by the kidneys, mainly (70%) unchanged. The half-life (T1/2) of moxonidine and metabolite is 2.5 and 5 hours, respectively. Despite its short half-life (about 3 hours), it controls blood pressure throughout the day [9]. Moxonidine is effective in monotherapy for hypertension, but it is optimal to prescribe it as part of combination therapy, for example, with ACE inhibitors, sartans (ARBs), thiazide diuretics and other main antihypertensive drugs. The combination of moxonidine with other antihypertensive drugs enhances their antihypertensive effect. Moxonidine, when added to therapy with an ARB II (eprosartan), normalizes blood pressure and sympathetic hyperactivity in hypertensive normovolemic patients with chronic renal failure. In terms of antihypertensive effectiveness, moxonidine is not inferior to diuretics, beta blockers, AK and ACE inhibitors, and in terms of tolerability it is significantly superior to previous centrally acting drugs. It is safer than clonidine, propranolol, captopril, nifedipine. Moxonidine improves the insulin sensitivity index by 21% (compared to placebo) in patients with obesity, insulin resistance and moderate hypertension. The sedative effect is significantly less pronounced than that of other centrally acting drugs. The drug potentiates the effects of central nervous system depressants - ethanol, tranquilizers, barbiturates. Moxonidine may moderately improve impaired cognitive function in patients receiving lorazepam. Prescribing moxonidine together with benzodiazepines may be accompanied by an increase in the sedative effect of the latter [1, 6, 8–10, 13–19].

The TOPIC (Trial Of Physiotens In Combination) study, conducted in the UK at 138 clinical sites, included 566 patients with hypertension aged 18–80 years. When prescribing moxonidine at a dose of 0.2 or 0.4 mg/day, reliable control with monotherapy was achieved in 294 (52%) patients, in the rest - with combination therapy (in combination with amlodipine or enalapril). During the study, the drug proved to be effective and well tolerated both in monotherapy and combination therapy [10, 11]. When using moxonidine in patients with hypertension, a dual mechanism of action is observed - the drug provides both short-term (mainly due to its effect on the sympathetic centers of the brain) and long-term (by suppressing the release of renin and improving excretory function of the kidneys) blood pressure control. Thus, a single oral dose of moxonidine (0.4 mg) caused a statistically significant decrease in blood pressure in patients with hypertension from an average of 176/105 mm Hg. Art. up to 158/95 mm Hg. Art. [10, 11].

For the treatment of patients with mild and moderate hypertension, the recommended initial dose of Moxarel (moxonidine) is 0.2 mg/day. If the response to treatment is unsatisfactory, after 2 weeks. the dose is doubled. A dose of 0.2–0.4 mg/day in most cases was sufficient to maintain blood pressure at a satisfactory level. The high antihypertensive efficacy of moxonidine has been confirmed in the treatment of patients with uncomplicated hypertensive crisis. Thus, with sublingual administration of moxonidine at a dose of 0.4 mg, an effective reduction in blood pressure with good tolerability of the drug was achieved in 90% of patients. A significant decrease in systolic blood pressure and diastolic blood pressure after a single dose of the drug is observed after 20 minutes and reaches a maximum after 1.5 hours [1, 2, 10, 12]. Moxarel (moxonidine) occupies a special place in the treatment of hypertension combined with obesity. By activating imidazoline I1 receptors, it helps reduce fat hydrolysis, reduce free fatty acids, increase glucose metabolism and increase insulin sensitivity, reduce triglyceride levels, increase high-density lipoproteins and reduce plasminogen activator inhibitor-1 levels. Studies have provided evidence of the effect of moxonidine on reducing insulin resistance in overweight patients with impaired glucose tolerance. Thus, in the comparative study ALMAZ, the effect of moxonidine and metformin on glycemic control in patients with overweight, mild hypertension, insulin resistance and impaired glucose tolerance was assessed. The criteria for inclusion of patients in the study were: age over 40 years, body mass index (BMI) >27 kg/m2, fasting glucose >6.1 mmol/l. The ALMAZ study showed that moxonidine lowered fasting glucose levels, reduced patients' weight, increased the rate of glucose utilization, and reduced insulin resistance. With moxonidine, fasting glucose levels decreased less pronounced than with metformin, but insulin levels significantly decreased, while metformin had no effect on it, and BMI decreased equally with both drugs. Both drugs statistically significantly increase insulin sensitivity after a glucose load. Moxonidine affects the level of insulin in the blood, metformin regulates glucose levels, which is accompanied by a decrease in glycosylated hemoglobin. Both drugs statistically significantly reduce body weight while remaining metabolically neutral to lipids [21–26].

Long-term therapy with moxonidine in elderly patients with hypertension of 1-2 degrees provides an optimal reduction in blood pressure during the day and at night with good tolerability of the drug (low frequency and insignificant severity of side effects), leads to a significant reduction in left ventricular hypertrophy, and a decrease in the left ventricular myocardial mass index. Monotherapy with moxonidine for 24 weeks. has a positive effect on cognitive functions (memory and thinking), which indicates improved functioning of the frontal lobes of the brain. In the field of intellectual activity, positive dynamics were observed - the ability of patients to perform actions that require a higher level of generalization in the visual-figurative and visual-logical spheres increased. In addition, during the treatment, positive changes in memory were revealed - the productivity of memorization increased [27]. For patients with metabolic syndrome, it is also important to note the nephroprotective effect of moxonidine. Long-term use of moxonidine causes a significant decrease in microalbuminuria, concentrations of free thrombomodulin and plasminogen activator inhibitor in the blood. According to the results of a post-marketing review study, moxonidine effectively reduces blood pressure in patients with metabolic syndrome and at the same time promotes weight loss in obese patients. After 8 weeks treatment, patients recorded a decrease in body weight by an average of 1.4 kg, with the most pronounced decrease observed in obese patients. The frequency of use of combination antihypertensive therapy was 81.1% among patients with metabolic syndrome and 63.3% in the group as a whole. There was a significant decrease in systolic (26.9±15.1 mmHg, 95% CI 26.4–27.3) and diastolic (13.2±9.5 mmHg, 95% CI 12 ,9–13.5) BP. High efficacy of moxonidine (diastolic blood pressure reduction to <90 mm Hg and/or diastolic blood pressure reduction >10 mm Hg) was reported in 94% of patients. Similarly, a positive effect was observed in a large number of patients with metabolic syndrome - 94%, obesity - 93%, diabetes - 94% and those receiving monotherapy - 95% [28–31].

Conclusions. Moxarel (moxonidine) is the drug of choice among antihypertensive drugs with a central mechanism of action and is characterized by high antihypertensive efficacy and tolerability in patients with overweight, obesity, metabolic syndrome or without it, and also has additional metabolic properties and has a beneficial effect on body weight. Moxonidine is well tolerated, has little interaction with other drugs and can be used once a day in most patients. Moxarel (moxonidine) is indicated for the treatment of patients with mild to moderate hypertension, and especially as an additional drug in the treatment of patients with metabolic syndrome.

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ESH-ESC Guidelines Committee. 2013 guidelines for the management of arterial hypertension // J. Hypertens. 2013. Vol. 31. P. 1281–1357. 8. Neumann J., Ligtenberg G., Oey L. et al. Moxonidine normalizes sympathetic hyperactivity in patients with chronic renal failure receiving eprosartan // J. Amer. Soc. Nephrol. 2004. Vol.15. P. 2902–2907. 9. Instructions (TCFS) for the drug Moxarel. 10. Gaponova N.I., Abdrakhmanov V.R., Baratashvili V.L., Tereshchenko S.N. Analysis of the effectiveness and safety of moxonidine in patients with arterial hypertension and hypertensive crises // Practical Medicine. Cardiology. 2011. 04. 11. Waters J., Ashford J., Jager BA et al. Use of moxonidine as unitial therapy and in combination in the treatment of essential hypertension: results of the TOPIC (Trial of Physiotens in Combination) study // J. Clin Basic Cardiol. 1999. Vol. 2. P. 219–224. 12. Ruksin V.V., Grishin O.V. Emergency care for high blood pressure that is not life-threatening // Cardiology. 2011. No. 2. P. 45–51. 13. Frei M., Küster l., Gardosch von Krosigk PP. et al. Moxonidine and hydrochlorothiazide in combination: a synergistic antihypertensive effect // J. Cardiovasc. Pharmacol. 1994. Vol. 24. P. 25–28. 14. Prichard BNC, Simmons R, Rooks MJ et al. A double-blind comparison of moxonidine and atenolol in the management of patients with mild – to moderate hypertension // J. Cardiovasc. Pharmacol.1992. Vol. 20. P. 45–49. 15. Wolf R. The treatment of hypertensive patients with a calcium antagonist or moxonidine: a comparison // J. Cardiovasc. Pharmacol. 1992. Vol. 20. P. 42–44. 16. Lotti G., Gianrossi R. Moxonidin vs. captopril in mild to moderate hypertension (German) // Fortschr. Med. 1993. Vol. 111 (27). P. 429–432. 17. Kraft K., Vetter H. Twenty – four – hour blood pressure profiles in patients with mild – to – moderate hypertension; moxonidine versus captopril // J. Cardiovasc. 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Analysis of efficacy and safety of moxonidine in patients with hypertension and hypertensive crises

Arterial hypertension (AH) is the most common disease in the Russian Federation.
At the same time, in our country there remains a steady trend of a steady increase in the number of emergency medical calls for hypertensive crises, which are the most serious complication of hypertension (1, 2, 3). Thus, in the Russian Federation as a whole, in recent years the number of calls from emergency medical teams for hypertensive crises (HC) has increased on average by 1.5 times, accounting for up to 20% of all reasons for calls (4.5%), and the total number of calls per year reaches 50 million (6.7). Thus, providing effective and, at the same time, safe emergency therapy to patients with hypertensive crises remains an urgent problem that requires constant analysis and improvement. In connection with the emergence of new antihypertensive drugs and the results of randomized multicenter studies, their introduction into practice will undoubtedly help improve the prognosis and quality of life of patients with hypertension.

Unfortunately, a number of antihypertensive drugs, while effectively lowering blood pressure, can have an unfavorable metabolic effect, thereby neutralizing the positive qualities of the drugs. Thus, beta-blockers, which successfully stop the hyperactivity of the sympathetic nervous system, can worsen carbohydrate metabolism, provoking hyperglycemia (up to the development of hyperglycemic coma in patients with diabetes mellitus (8). By provoking bronchospasm, beta-blockers can worsen the course of bronchial asthma and chronic obstructive diseases .

Due to the leading role of sympathetic hyperactivity in the development of arterial hypertension and hypertensive crises, new generation sympatholytics, such as moxonidine and rilmenidine, have recently been actively introduced into clinical practice.

Sympatholytics

Sympatholytics reduce blood pressure by exerting a selective effect on the vasomotor centers of the medulla oblongata, which provide regulation of sympathetic tone (11, 12, 13). This pharmacological group originates from methyldopa and clonidine, later moxonidine (physiotens) and rilmenidine were synthesized. Due to differences in the points of application and pharmacological effects, sympathomimetics are usually divided into drugs of the first generation or “old” and drugs of the second generation or “new”.

As can be seen from table. 1 and fig. 1, methyldopa affects exclusively alpha2-adrenergic receptors located on the neurons of the nuclei of the solitary tract of the medulla oblongata. Clonidine is a mixed agonist, since, along with alpha2-adrenergic receptors, it also has the ability to stimulate I1-imidazoline receptors located in the ventrolateral parts of the medulla oblongata (14).

Table 1.

Points of application of the effects of sympatholytics

Figure 1. Points of application and antihypertensive effect of sympatholytics

Second generation drugs are selective agonists of I1-imidazoline receptors. In contrast to the “old” sympathomimetics, the new drugs, especially moxonidine, have low affinity for alpha2-adrenergic receptors in the brainstem (15, 16). As a result, the risk of side effects such as sedation and dry mouth is significantly reduced.

The selectivity of moxonidine for I1-imidazoline receptors is approximately 70 times greater than its selectivity for alpha2-adrenergic receptors, while rilmenidine is less selective and therefore less effective (17). It is also known that the interaction of centrally acting drugs with alpha2-adrenergic receptors in brain areas is responsible for problems associated with the development of side effects (sedation, depression, dry mouth, etc.) characteristic of “old” sympathomimetics (18, 19, 20). At therapeutic doses, moxonidine has no side effects and causes a dose-dependent decrease in blood pressure without the development of withdrawal syndrome and with a slight change in heart rate (21). A decrease in plasma renin levels and an increase in natriuresis was also detected, which is probably mediated by stimulation of imidazoline receptors in the kidneys (22).

Moxonidine reduces plasma levels of renin, angiotensin II, and aldosterone (22). These effects are of particular importance, since a decrease in the activity of the renin-angiotensin-aldosterone system (RAAS) prevents the development and progression of cardiac and vascular remodeling (23, 24, 25, 26).

A decrease in the hyperactivity of the sympathetic nervous system during treatment with moxonidine is accompanied by an increase in tissue sensitivity to insulin, an improvement in carbohydrate and lipid metabolism, in particular, a decrease in the level of plasma glucose and serum leptin (27, 28). The positive effect of moxonidine on carbohydrate and lipid metabolism makes it the drug of choice for the treatment of hypertension in patients suffering from diabetes mellitus and metabolic syndrome.

According to numerous double-blind randomized studies, moxonidine was not inferior in antihypertensive effectiveness to diuretics, beta-blockers, calcium antagonists and ACE inhibitors, and in tolerability it was significantly superior to previous centrally acting drugs (29-35).

It is important to note the stability of the antihypertensive effect of moxonidine - the ratio of the residual reduction in blood pressure to the maximum reduction in blood pressure - this figure should be at least 50%. For moxonidine it is 70%.

When using moxonidine in patients with hypertension, a dual mechanism of action is observed - the drug provides both short-term (mainly due to its effect on the sympathetic centers of the brain) and long-term blood pressure control (due to suppression of renin release and improvement of renal excretory function). Thus, a single oral dose of moxonidine (0.4 mg) caused a statistically significant decrease in blood pressure in patients with hypertension from an average of 176/105 mm Hg. Art. up to 158/95 mm Hg. Art. (36). At the same time, the antihypertensive effect of the drug was accompanied by a decrease in the initially elevated total vascular resistance from 1695 to 1427 dynes. sec/cm5, while cardiac output did not change significantly (Fig. 2).

Figure 2. Effect of moxonidine on cardiac output and total vascular resistance (according to V. Mitrovic et al., 1991)

An interesting feature of moxonidine was also revealed: in patients with hypertension, a higher initial blood pressure level is associated with a stronger decrease in blood pressure. In this regard, the possibility of relieving hypertensive crises with moxonidine is considered a promising area of ​​application in clinical practice. In addition, the effectiveness and safety of the use of moxonidine in hypertension and a number of concomitant diseases, such as chronic obstructive pulmonary disease (COPD), diabetes mellitus, metabolic syndrome, etc., is noted.

Pharmacokinetics of moxonidine

When taken orally, absorption of moxonidine from the gastrointestinal tract is 90% (37). The maximum concentration in blood plasma after a single dose of 0.2 mg of the drug is achieved after 60 minutes. (36, 37). Bioavailability - 88%. Food intake does not affect the pharmacokinetics of moxonidine. The half-life of moxonidine and metabolites is 2.5 and 5 hours, respectively. Within 24 hours, more than 90% of the drug is excreted by the kidneys (37). Moxonidine does not accumulate with long-term use.

Repeated administration of moxonidine does not lead to accumulation in the body of patients, including patients with moderate renal failure (39). In the later stages, in patients with end-stage renal failure (creatinine clearance less than 10 mg/min) on hemodialysis, plasma concentrations and final plasma half-life (T1/2) are 6 and 4 times higher, respectively. than in patients with normal renal function. In such patients, the dose of the drug should be selected individually. Encouraging results confirming the renoprotective properties of moxonidine were obtained by J. Radermacher et al. (40). In 601 patients undergoing renal allotransplantation, moxonidine therapy resulted in a 70% reduction in the risk of allograft failure.

Use of moxonidine in clinical practice

The TOPIC (Titial of Physiotens in Combination) study, conducted in the UK at 138 clinical sites (42), included 566 hypertensive patients aged 18–80 years. When prescribing moxonidine at a dose of 0.2 mg or 0.4 mg per day, reliable control with monotherapy was achieved in 294 patients (52%), in the remaining patients - with combination therapy (in combination with amlodipine or enalapril). During the study, the drug proved to be effective and well tolerated both in monotherapy and in combination therapy.

The high antihypertensive efficacy of moxonidine has been confirmed in the treatment of patients with uncomplicated hypertensive crisis. Thus, with sublingual administration of moxonidine at a dose of 0.4 mg, an effective reduction in blood pressure with good tolerability of the drug was achieved in 90% of patients (5). As can be seen in Fig. 3, a significant decrease in systolic blood pressure and diastolic blood pressure after a single dose of the drug is observed after 20 minutes and reaches a maximum after 1.5 hours.

Figure 3. Changes in SBP (a) and DBP (b) with sublingual application of 0.4 mg moxonidine: before treatment (0); after 20 and 30 minutes; 1.5 and 3 hours after administration (according to V.V. Ruksin and O.V. Grishin, 2011)

SBP—systolic blood pressure; DBP - diastolic blood pressure

It is important to note that the examined patients did not have rebound syndrome, and dynamic monitoring of blood pressure levels confirmed the stable and long-term nature of the antihypertensive effect of moxonidine.

A positive effect of moxonidine on the course of hypertension was revealed in the treatment of patients who are very difficult to treat with antihypertensive therapy, namely, patients with COPD (43). As a rule, beta-blockers, as well as ACE inhibitors, which can provoke coughing and increased bronchial obstruction, are contraindicated in such patients. In a study of 40 patients with arterial hypertension due to COPD, treatment with moxonidine was accompanied by an improvement in the hemodynamics of the systemic and pulmonary circulation. Thus, the decrease in systolic blood pressure and diastolic blood pressure was 15.4 and 17.4%, respectively, reaching normal values. The pulse rate remained within normal limits during treatment and did not change significantly.

Thus, the selective inhibitor of I1-imidazoline receptors moxonidine (Physiotens) can be used as a universal antihypertensive drug, effective both for relieving hypertensive crises and for long-term treatment of arterial hypertension. Unlike “old” centrally acting drugs such as clonidine, methyldopa, moxonidine does not cause serious adverse events; There are also no hypotensive effects of the “first dose” and rebound syndrome. Moxonidine may be considered the drug of choice for the treatment of arterial hypertension and uncomplicated hypertensive crises in patients with diabetes mellitus, metabolic syndrome and chronic obstructive pulmonary diseases.

Since 2010, under the auspices of the VNOK section “Emergency Cardiology,” a randomized multicenter comparative study of the effectiveness of moxonidine in patients with uncomplicated hypertensive crisis has been conducted. The study is being conducted at 14 clinical centers in different regions of the Russian Federation. The study plans to include 280 patients with uncomplicated hypertensive crisis who are in the hospital at the time of inclusion in the study. Patients were randomized into two groups: group 1 (n=140) received a single oral dose of moxonidine at a dose of 400 mcg, control group 2 (n=140) received captopril at a dose of 25 mg. The duration of observation of the effect of moxonidine and captopril is 24 hours. The results of this study will be published this year.

N.I. Gaponova, V.R. Abdrakhmanov, V.L. Baratashvili, S.N. Tereshchenko

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