This product is a dihydropyridine calcium channel blocker. It reversibly competes with nitrendipine and (or) other calcium channel blockers for dihydropyridine binding sites, blocks voltage-dependent Ca2 currents in vascular smooth muscle and cultured rabbit atrial cells, and blocks K-induced rat portal vein contracture. In vitro studies have shown that felodipine has a stronger selective inhibitory effect on vascular smooth muscle than on myocardium; negative inotropic effects can be detected in vitro, but this effect has not been observed in whole animals. Felodipine reduces blood pressure by reducing peripheral vascular resistance. This pharmacological effect is dose-related and accompanied by a reflex increase in heart rate. The antihypertensive effect of felodipine is dose-dependent and positively correlated with blood drug concentration. Felodipine does not affect the P-R interval of the electrocardiogram when used alone or in combination with beta-blockers. Clinical studies and electrophysiological studies have shown that felodipine alone or in combination with beta-blockers has no significant effect on cardiac conduction (P-R, P-Q and H-V intervals). The antihypertensive treatment of felodipine is associated with a significant recovery of pre-existing left ventricular hypertrophy. Felodipine can reduce the reabsorption of filtered sodium by the renal tubules to produce natriuretic and diuretic effects, eliminate the common sodium and water retention effects of other vasodilators, and do not affect daily potassium excretion. Felodipine reduces renal vascular resistance, normal glomerular filtration rate remains unchanged, and the glomerular filtration rate of patients with renal impairment will increase. Felodipine does not affect the excretion of urinary albumin, and can play an anti-anginal and anti-ischemic role by improving myocardial oxygen supply. It reduces coronary vascular resistance by dilating epicardial arteries and arterioles, increases coronary blood flow and myocardial oxygen supply, and effectively relieves coronary spasm. The decrease in peripheral blood pressure caused by felodipine reduces left ventricular afterload and myocardial oxygen demand. For stable exertional angina pectoris, felodipine can improve exercise tolerance and reduce angina attacks; for patients with vasospastic angina pectoris, it can reduce the occurrence of symptomatic and painless myocardial ischemia.

This product is a dihydropyridine calcium channel antagonist (calcium channel blocker), which acts by reversibly competing for dihydropyridine binding sites, blocking the voltage-dependent Ca2 current of vascular smooth muscle and cultured rabbit atrial cells, and blocking K-induced rat portal vein contracture.

Relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), increases cyclic guanosine monophosphate (cGMP), regulates the contractile state of smooth muscle, and causes vasodilation; dilates the arteriovenous bed mainly by dilating the veins, reduces the amount of blood returning to the heart and left ventricular end-diastolic pressure (preload), reduces peripheral resistance (afterload), reduces myocardial oxygen consumption, and relieves angina pectoris; has a dilating effect on epicardial coronary artery branches; may affect the effective coronary perfusion pressure when lowering blood pressure; reduces central venous pressure and pulmonary capillary wedge pressure, pulmonary vascular resistance and systemic vascular resistance, slightly increases heart rate, and may change the cardiac index.

Centrally acting antitussive drugs can effectively relieve cough symptoms

It can promote the secretion of mucus in the bronchi, thin the sputum, and make it easier to cough up the sputum.

Has bronchodilator and antitussive effects

Antihistamines, which have anti-allergic effects

The main pharmacological action is to relax vascular smooth muscle. Nitroglycerin releases nitric oxide (NO), which is the same as endothelial relaxing factor, activating guanylate cyclase, increasing cyclic guanosine monophosphate (cGMP) in smooth muscle and other tissues, leading to dephosphorylation of myosin light chain, regulating the contractile state of smooth muscle, and causing vasodilation.