Gou Teng

Ramulus Uniariae cum Unus, Gastradia Tuber

Dosage

6-30g, decoction, pill or powder.

Toxicity

LD50 (mice/ rhynchophyline/abdominal injection): 162.3mg/kg; LD50 (mice/total alkaloid hydrochloride): 514.6 ± 29.1mg/kg (oral) and 144.2 ± 3.1mg/kg (abdominal injection). (1) 4 Given a dose of 50mg/kg or 100mg/kg for two consecutive months, the group with low dosage suffered from mild dystrophy in kidney, and the group with high dose suffered from significant pathogenic in heart, liver, and kidney. (2)

Chemical Composition

Yohimbine; Heteroyohimkin; Uncaramine; Callophylline; Roxburghines A, B, C, P, E, and X; Corynoxine; Corynoxine B; Rhynophylline; Isocorynoxeine; Isorhynchophyllic acid methylester; Corynoxeine; Rhynchophyllic acid methylester; Hirsuteine; Hirsutine; Corynantheine; Dihydrocorynantheine; Akuammicine; Rhynchonhine; Vincoside lactam; Strictosamide; Isovincoside lactam; Vallesiachotamine; Epicatechin; Hyperin; Trifolin; Isopteropodine; Mitraphylline; Isorhynchophychophyllic acid; Rhynchophylline; Tetrahydroalstonine; Isoformosanine; Isorhynchophylline N-oxide; Pteropodine N-oxide; Rhynchophylline N-oxide; Mitraphylline N-oxide; Mitraphylline N-oxide; Scopoletin; Hydroxy-indole alkoloid. (3) , (4) , (5) , (6) , (7) , (8)

Pharmacology

Effects on hypertension and hyperlipidemia

Administered at 10g/kg daily to rats with spontaneous hypertension, the water decoction of Gou Teng can lower the blood pressure after four consecutive weeks of administration; at the end of eight weeks, there is a notable improvement in serum cholesterol, high-density lipoprotein, b-lipoprotein, triglyceride, and the A/G ratio. (9) Compound Gou Teng can lower the blood pressure of rats of apoplexy or spontaneous hypertension. Administered to rats of experimental hyperlipidemia, compound Gou Teng can lower the levels of serum TC, LDL-C, and TG, while raising the level of HDL-C. (10)

Effects on the heart

Rhynchophylline can inhibit myocardial contraction and decrease myocardial oxygen consumption. (11) Administered at 8mg/kg by IV injection, one dose of isorhynchophylline sees its inhibitory effect peak at the five-minute mark and disappear after 30-120 minutes. Administered at 0-16mg/kg, isorhynchophylline has the following dose-dependent effects: lowering the heart rate; prolonging the sinoatrial node’s recovery time, the sinoatrial conductive time, the interval between the cardiac atrium and Keith’s bundle, the interval between Keith’s bundle and the cardiac ventricle, and the P-R interval in electrocardiogram. Among these, the inhibition on atrioventricular conduction is significant. (12) Moreover, isorhynchophylline has a concentration-dependent inhibitory effect on the spontaneous frequency and contractility of the cardiac atrium in guinea pigs. (13)

Effect on platelet aggregation and thrombus formulation

Administered to rats, rhynchophylline can significantly suppress platelet aggregation induced by AA, collagen, and ADP. It does not keep platelets from utilizing the exogenic AA to synthesize TXA2, but it does inhibit collagen-induced production of TXA2. It has been shown that at the effective dosage for inhibition, it has no effect on the production of PG12. (14) While rhynchophylline can, in rabbits, inhibit the forming of thromboxane B2 by collagen-induced platelets, it does not affect AA-induced production of thronboxane B2. (15)

Sedative Effect

Gou Teng total alkaloids can effect a significant nerve conduction block, infiltration anesthesia, and intraspinal anesthesia. This effect is both pronounced and immediate, and lasts 90 ± 15 minutes. (16) Experiments on mice show that rhynchophilline decreases spontaneous activity, strengthens phentobarbital-induced sedative effect, and increases the content of 5-HT in the hypothalamus and the amygdaloid nucleus. (17)

Effects on smooth muscles

Research shows that 1) rhynchophilline decreases K+- and Na+-induced smooth muscle contractions, with the effect being significantly more pronounced on K+-induced contraction than on a Na+-induced one; 2) it decreases the release of Ca2+ in Na+-induced contractions, resulting in a rightward shift in the dose-effect curves of K+ , Na+ and Ca2+. It blocked the flow of Ca+ inside or outside; and 3) it blocks the bi-directional flow of Ca2+. (18)

References

  1. Chinese Materia Medica. Shanghai: Science and Technology Press; 1998.
  2. Zhang Jian Jun, et al. Journal of Chinese Patented Medicine. 1999;21(4):177-178.
  3. Liu Gui, et al. China Journal of Pharmacy. 1991;26(10):583-590.
  4. Zhang Ling, et al. Journal of Chinese Materia Medica. 1998;19(10):649-651.
  5. Zhang Jun, et al. Journal of Chinese Materia Medica. 1999;30(1):12-14.
  6. Chinese Materia Medica. Shanghai: Science and Technology Press; 1998.
  7. Liu Hong Mei, et al. Journal of Chinese Materia Medica. 1993;24(2):61-63.
  8. Shi Yu Jun. Journal of Chinese Materia Medica. 1994;25(12):653.
  9. Chu Jie, et al. Journal of Pharmacology and Clinical Application of TCM. 1993;9(4):14-16.
  10. Wang Yu Fen, et al. Journal of Pharmacology and Clinical Application of TCM. 1993;9(6):11-12, 10.
  11. Zhang Wei, et al. China Journal of Pharmacology. 1986;7(5):426.
  12. Sun An Sheng, et al. China Journal of Pharmacology and Toxicology. 1995;9(2);113-115.
  13. Zhu Yi, et al. Chinal Journal of Chinese Medicine. 1995;20(2):112-114.
  14. Jin Ruo Ming, et al. Journal of Pharmacology. 1991;26(4):246-249.
  15. Chen Chang Xun, et al. China Journal of Pharmacology. 1992;13(2):126-130.
  16. Zhang Xin An, et al. Journal of Clinical Application in Anesthesiology. 1999;15(1):25-26.
  17. Shi Jing Shan, et al. China Journal of Pharmacology. 1993;14(2):114-117.
  18. Zhang Wei, et al. China Journal of Pharmacology. 1987;(5):425-429.