Combined antihypertensive drug. The effect is due to the action of two components - beta1-adrenoblocker (atenolol) and a blocker of "slow" calcium channels, (amlodipine).
A fixed combination of atenolol and amlodipine is considered the most effective combination when viewed from the standpoint of hemodynamic and metabolic drug interactions. Reception of Amlodipine leads to d, dilatation of arterioles, expressed reflex tachycardia.This is one of the main side effects of amlodipine. An increase in heart rate leads to an increase in myocardial oxygen demand, which is undesirable for patients with ischemic heart disease. Being a selective blocker pi-adrenergic receptors, Atenolol it neutralizes the reflex tachycardia caused by the administration of amlodipine.
Clinical studies of recent years have demonstrated the beneficial effect of blocking "slow" calcium channel blockers on the lipid spectrum of blood, which helps reduce the risk of cardiovascular outcomes. The complementary mechanism of the action of amlodipine, which reduces the overall peripheral resistance of blood vessels and Atenolol, reduces cardiac output, leads to a more pronounced hypotensive effect and better tolerability than monotherapy with amlodipine and atenolol, improving the efficiency / side effect ratio.
Atenolol: has antianginal, hypotensive and antiarrhythmic act. Does not possess membrane stabilizing and internal sympathomimetic activity.Reduces the stimulation of catecholamines formation of cAMP and ATP, reduces the intracellular current of Ca2+. In the first 24 hours after oral administration, with a decrease in cardiac output, there is a reactive increase in the total peripheral resistance of blood vessels, the severity of which decreases gradually over the course of 1-3 days.
The hypotensive effect is associated with a decrease in cardiac output, a decrease in the activity of the renin-angiotensin system, the sensitivity of barocereptors, and effects on the central nervous system. The hypotensive effect is manifested by a decrease in systolic and diastolic arterial pressure, a decrease in the impact and minute volumes. In average therapeutic doses, it has no effect on the tone of peripheral arteries. The hypotensive effect lasts 24 hours, with regular admission is stabilized by the end of 2 weeks of treatment.
The antianginal effect is determined by the reduction in myocardial oxygen demand as a result of a decrease in the heart rate (diastolic elongation and improvement of myocardial perfusion) and contractility, as well as a decrease in myocardial sensitivity to sympathetic innervation.It reduces the heart rate at rest and during physical activity. By increasing the tension of the ventricular muscle fibers and the final diastolic pressure in the left ventricle, it can increase the demand for myocardium in oxygen, especially in patients with chronic insufficiency. The antiarrhythmic effect is manifested by suppression of sinus tachycardia and is associated with the elimination of arrhythmogenic sympathetic influences on the conduction system of the heart, inhibition of heterogeneous automatism, a decrease in the rate of propagation of excitation through the sinouauricular node, and an extension of the refractory period. Oppresses the impulses in antegrade and, to a lesser extent, in retrograde directions through the atrioventricular node and along additional paths.
Increases the survival rate of patients who underwent myocardial infarction (reduces the incidence of ventricular arrhythmias and strokes of the stecardia).
In therapeutic concentrations does not affect beta-2 adrenergic receptors, in contrast to non-selective beta-adrenoblockers has a less pronounced effect on the smooth muscles of the bronchi and peripheral arteries and on lipid metabolism.Slightly reduces the vital capacity of the lungs, almost does not weaken the bronchodilating effect of isoproterenol. When taking more than 100 mg per day, it can have a beta-2-adrenergic blocking effect. Negative chronotropic effect is manifested 1 hour after admission, reaches a maximum after 2-4 hours and lasts up to 24 hours.
Amlodipine: a dihydropyridine derivative. Has antihypertensive, antianginal, antispasmodic and vasodilating action. It blocks the flow of calcium ions through the cell membranes into the smooth muscle cells of the myocardium and vessels.
The mechanism of hypotensive action is caused by a direct relaxing effect on the smooth muscles of the vessels.
The antianginal effect of the drug is due, first, to its ability to expand the peripheral arterioles, which leads to a decrease in the overall peripheral vascular resistance. Reducing the burden on the heart leads to a decrease in myocardial oxygen demand. Secondly, the effect of the drug, due to the expansion of the coronary arteries, increases the flow of oxygen into the myocardium (especially with vasospastic angina). Amlodipine does not adversely affect the metabolism and lipids of blood plasma, has antiatherosclerotic, antithrombotic activity, increases the rate of glomerular filtration, has a weak natriuretic effect. When diabetic nephropathy does not increase the severity of microalbuminuria.