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About This Product
Manufacturer
Merck Sp. z o.o.
ATC Code
C07FB07
Source
URPL
Pharmacotherapeutic group: selective beta-blockers and other antihypertensives. ATC code: C07FB07
Mechanism of action of amlodipine:
Amlodipine inhibits the transmembrane influx of calcium ions into cardiac and vascular smooth muscle (slow calcium-channel blocker or calcium ion antagonist).
The antihypertensive action of amlodipine is due to a direct relaxant effect on vascular smooth muscle, leading to a reduction in peripheral vascular resistance.
The precise mechanism by which amlodipine relieves anginal pain has not been fully elucidated, but it may act in the following two ways:
By dilating peripheral arterioles, thereby reducing total peripheral resistance (afterload).
Because amlodipine does not produce reflex tachycardia, myocardial energy expenditure and oxygen demand are reduced.
By dilating the main coronary arteries and coronary arterioles in both normal and ischaemic regions, oxygen supply is improved. Through this mechanism, amlodipine also enhances oxygen delivery to the myocardium in patients with coronary artery spasm (Prinzmetal's or variant angina).
Pharmacodynamic properties of amlodipine:
In hypertensive patients, once-daily dosing of amlodipine produces clinically significant reductions in blood pressure in both supine and standing positions over a 24-hour period. Owing to its slow onset of action, amlodipine does not cause acute hypotension.
In patients with angina, a single daily dose of amlodipine increases total exercise tolerance, delays the onset of anginal pain and significant ST-segment depression, and reduces both the frequency of anginal attacks and nitroglycerin consumption.
Amlodipine has not been associated with any adverse metabolic effects: it has no effect on plasma lipids, blood glucose or serum uric acid, and is suitable for use in patients with asthma.
Mechanism of action of bisoprolol:
Bisoprolol is a highly potent beta1-selective adrenoceptor blocker without intrinsic sympathomimetic activity (ISA) or membrane-stabilising activity.
It exhibits only low affinity for beta2-receptors of bronchial and vascular smooth muscle and for beta2-receptors involved in metabolic regulation. Consequently, bisoprolol is generally not expected to affect airway resistance or beta2-mediated metabolic effects. Its beta1-selectivity extends beyond the therapeutic dose range. Bisoprolol does not have a marked negative inotropic effect.
Bisoprolol reaches its peak effect 3–4 hours after oral administration. With an elimination half-life of 10–12 hours, it provides a 24-hour effect after once-daily dosing. Maximum antihypertensive efficacy of bisoprolol is generally achieved after 2 weeks.
On acute administration to patients with ischaemic heart disease without chronic heart failure, bisoprolol reduces heart rate and stroke volume, thereby decreasing cardiac output and oxygen consumption. With long-term administration, the initially elevated peripheral resistance declines.
The antihypertensive effect of beta-blockers is, among other factors, attributable to a reduction in plasma renin activity.
Pharmacodynamic properties of the fixed-dose combination:
This combination enhances the antihypertensive and antianginal effect through the complementary mechanisms of its two active substances: the vasoselective action of amlodipine as a calcium-channel blocker (reduction of peripheral resistance) and the cardioselective action of bisoprolol as a beta-blocker (reduction of cardiac output).
⚠️ Warnings
Associated with amlodipine:
The safety and efficacy of amlodipine in hypertensive crisis have not been established.
Heart failure
Patients with heart failure should be treated with caution. In a long-term placebo-controlled study in patients with severe heart failure (NYHA class III and IV), a higher incidence of pulmonary oedema was reported in the amlodipine group than in the placebo group, although this was not associated with worsening of heart failure. Calcium-channel blockers, including amlodipine, must be used with caution in patients with heart failure due to an increased risk of further cardiovascular events and mortality.
Hepatic impairment
The elimination half-life of amlodipine is prolonged and AUC values are higher in patients with impaired hepatic function; dosing recommendations have not been established. Amlodipine should therefore be administered with caution in these patients.
Elderly patients
In elderly patients, the dose should be increased with caution (see section 5.2).
Renal impairment
Amlodipine may be used at standard doses in these patients. Changes in plasma amlodipine concentrations are not correlated with the degree of renal impairment. Amlodipine is not dialysable.
Associated with bisoprolol:
Particularly in patients with ischaemic heart disease, treatment must not be discontinued abruptly unless clearly indicated, as this may cause transient deterioration of the underlying cardiac condition (see section 4.2).
Bisoprolol should be administered with particular caution in patients with hypertension or angina pectoris associated with heart failure.
Bisoprolol must be used with caution in:
diabetes mellitus with marked fluctuations in blood glucose; symptoms of hypoglycaemia (e.g. tachycardia, palpitations or sweating) may be masked;
strict diet, fasting;
ongoing desensitisation therapy. As with other beta-blockers, bisoprolol may increase both the sensitivity to allergens and the severity of allergic reactions. Adrenaline treatment may not always produce the expected therapeutic effect;
first-degree AV block;
Prinzmetal's angina. Cases of coronary vasospasm have been observed. Despite its high beta1-selectivity, anginal attacks cannot be entirely excluded when bisoprolol is given to patients with Prinzmetal's angina;
peripheral arterial occlusive disease (an aggravation of complaints may occur, especially when treatment is initiated);
in patients with psoriasis or a history of psoriasis, beta-blockers (e.g. bisoprolol) should be used only after careful consideration of the risk-benefit ratio;
symptoms of hyperthyroidism may be masked during bisoprolol treatment;
in patients with phaeochromocytoma, bisoprolol must not be administered until alpha-adrenergic receptor blockade has been established;
in patients undergoing general anaesthesia; beta-blockers reduce the incidence of arrhythmias and myocardial ischaemia during induction of anaesthesia, intubation and the postoperative period. Continued maintenance dosing of beta-blockers is currently recommended. The anaesthetist must be informed of beta-blocker use because of potential interactions with other medicines that may result in bradyarrhythmias, attenuation of reflex tachycardia and reduced reflex capacity to compensate for blood loss. If discontinuation of beta-blocker therapy is considered necessary prior to surgery, withdrawal must be gradual and completed approximately 48 hours before anaesthesia.
Although cardioselective (beta1) beta-blockers may have less impact on lung function than non-selective beta-blockers, their use should be avoided (as with all beta-blockers) in patients with obstructive airways disease unless there is a compelling clinical reason. Where such a reason exists, bisoprolol may be administered with caution. In the case of bronchial asthma or other chronic obstructive pulmonary disease that may produce symptoms, concomitant bronchodilator therapy should be given. In asthmatic patients, an increase in airway resistance may occasionally occur, requiring an increase in the dose of β2-stimulants.
Sodium
This medicinal product contains less than 1 mmol (23 mg) sodium per tablet, that is to say essentially "sodium-free".
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Verified by medical editor
Dr. Ozarchuk, PharmD · April 2026
Source: РЛС РФ · rlsnet.ru
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