Rhynchophylline is an alkaloid found in certain Uncaria species (Rubiaceae), notably Uncaria rhynchophylla, Uncaria tomentosa and Gambirplant (Gouteng). The total alkaloid content in Uncaria rhynchophyl-lina is about 0.2 %, in which rhynchophylline (Rhy) is 28 %-50 %, isorhynchophylline is 15 %. The pharmacological effects of Rhynchophylline and Isorhynchophylline were extensively studied, especially in the cardiovascular system. The hypotensive effect of Rhynchophylline was also observed in 1978. The peculiarity of Rhynchophylline was that renal blood flow was not significantly interfered upon lowering of blood pressure. Although the effect of Rhynchophylline on the renin secretion remained unclear, the consequence of Rhynchophylline on the renal blood flow ought to be considered as an advantage. The cardiovascular effects of Rhy were supposed due to calcium channel block. In an experiment with the guinea pig, Rhy inhibited the left atrium post-rest potential enhancement and staircase phenomenon. The post-rest potential enhancement induced by Auxo-frequency stimulation is the characteristic of Ca(‘2+) influx increase, and the calcium antagonists, such as verapamil, can reverse the staircase phenomenon. In isolated strips of rabbit aorta, Rhynchophylline inhibited 45Ca(‘2+) influx induced by K(‘+). Effects of Rhynchophylline on the 45Ca2+ influx and efflux induced by noradrenaline were small. The vasodilative effect of Rhynchophylline was mainly due to the dysfunction of Ca(‘2+) transport, including the influx of extracellular calcium and release of intracellular calcium by blocking the voltage-dependent calcium channel and the receptor-regulation calcium channel. Brachycardia and cardiac contractility repression induced by Rhynchophylline were observed. Rhynchophylline inhibited rabbit platelet aggregation induced by arachidonic acid (AA), collagen, and ADP, and reduced the thromboxane B2 (TXB2) generation in platelet-rich plasma (PRP) induced by collagen but failed to reduce TXB2 generation that induced by AA. Rhynchophylline suppressed malondialdehyde (MDA) formation in platelet suspension stimulated by thrombin, inhibited the platelet factor 4 (PF4) release. It did not alter intraplatelet cAMP concentration. Rhynchophylline 10-20 mg/kg iv showed a significant inhibition of venous thrombosis and cerebral thrombosis in rats. Rhynchophylline can relieve contraction of the respiratory tract smooth muscle and uterus smooth muscle induced by the agonist, in which a mechanism of calcium channel blocking was also proposed. In a cultured brain slice of rats, Rhynchophylline increased the 5-HT content in the hypothalamus and cortex but reduced the dopamine (DA) concentrations in the cortex, amygdala, and spinal cord. Rhynchophylline promoted the release of endogenous DA from hypothalamus, cortex, amygdala, and spinal cord. The release of 5-HT was increased in cortex and amygdala and was decreased in hypothalamus slice. However, Rhynchophylline inhibited the release of both 5-HT and DA evoked by high potassium. Rhynchophylline can protect neurons from damage induced by dopamine, which behaves as a free radical at higher concentration.