Liensinine 5mg/kg, iv, can significantly inhibit the arrhythmia induced by aconitine in rats and waabain in guinea pigs; It can also prevent the occurrence of epinephrin-induced ventricular fibrillation in guinea pigs and prevent the arrhythmia caused by myocardial ischemia and reperfusion in rats. Liensinine 85mg/kg iv can slow down the heart rate and prolong the P-R interval in rabbits; Liensinine 30μmol/L can prolong the left atrial functional refractory period in isolated guinea pigs. Liensinine slows down heart rate, prolongs ventricular diastolic period, facilitates blood perfusion from epicardial region to intimal region, and improves ischemia and hypoxia. Inhibit myocardial contraction, reduce afterload, and thus reduce myocardial oxygen consumption, which is conducive to the anti-arrhythmic effect. Liensinine has effects on slow response action potential and slow inward current of myocardium. 10-100 μmol/L can reduce slow response action potential amplitude (APA) and zero phase maximum rise rate (Vmax) of isolated rabbit sinus node (SAN) pacemaker cells in a concentration-dependent way, and prolong sinus perimeter (SCL), which is stronger than quinidine at the same concentration. It also significantly antagonized Bayk8644, increased the APA and Vmax effects of SAN pacing cells and the slow response action potential induced by high K+ in guinea pig papillary muscle, and inhibited the slow inward-flowing of canine Purkinje fibers in a concentration-dependent way by liensinine from 1 to 100μmol/L. It can also counteract the effect of acetylcholine on shortening action potential duration, which suggests that liensinine can inhibit the transmembrane transport of Na+, K+ and Ca2+. It was found that liensinine can block L-type calcium channel currents in guinea pig ventricular myocytes in a concentration-dependent manner, which may be one of the important mechanisms of liensinine's resistance to various experimental arrhythmias. Liensinine has a transient antihypertensive effect. After intravenous injection of liensinine 10mg/kg, the blood pressure immediately dropped to 40% of the original level, and the electrocardiogram showed tachycardia, but it recovered in 10min to 20min. About 20 minutes after the duodenal administration of 100mg/kg, the blood pressure began to drop, observed for 2 hours, the blood pressure dropped to 30% of the original level, the heart rate slowed down. The antihypertensive effect and effective action time of liensinine are dose-dependent, and the antihypertensive effect is basically the same as that of methyl liensinine (another alkaloid extracted from lotus seed heart), but the effective action time is shorter than that of methyl liensinine. The results showed that the effect of liensinine on diastolic blood pressure was greater than that on systolic blood pressure, suggesting that the main site of action of liensinine was in peripheral blood rather than central. Inhibition of smooth muscle contraction liensine had different inhibitory effects on the contraction of aorta ring induced by deoxyadrenaline (PE), 5-hydroxytryptamine (5-HT) and histamine (His), and the inhibitory effect on the contraction induced by PE was more obvious. The inhibition of shrinkage induced by high K+ depolarization was not obvious, suggesting that the drug had little effect on voltage-dependent calcium channels. Lienine can also inhibit the contraction of urethral smooth muscle induced by PE. On the isolated rabbit aortic ring and the rat anorectal muscle, the α1 receptor agonist methoxyamine and PE dose-effect curve can be shifted parallel to the right, and the maximum response remains unchanged. The PA2 values measured were 6.8 and 6.6, respectively, indicating that lienine has high selectivity and competitive antagonism to α1 receptor. It also significantly inhibited the endogenous calcium release caused by norepinephrine (NE), but had little effect on the exogenous calcium flow caused by NE, and had the effect of inhibiting the intracellular calcium release.