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Influence of Ginseng Saponins on the Isolated Aortic Contractile Response of the Spontaneously Hypertensive Rat

  • Lim, Dong-Yoon (Department of Pharmacology, College of Medicine, Chosun University) ;
  • Cha, Dong-Seok (Department of Pharmacology, College of Medicine, Chosun University)
  • Published : 2002.12.01

Abstract

The present study was attempted to investigate the effects of total ginseng saponin (G75), panaxadiol-type (PDS) and panaxatriol-type saponin (PTS) on contractile responses of vasoconstrictors in aortic smooth muscle stripes of normotensive (NR) and spontaneous hypertensive rats (SHR). Phenylephrine (an adrenergic $\alpha$$\_$1/-receptor agonist) and high potassium (a membrane depolarizing agent) caused greatly contractile responses in both NR and AHR aorta, respectively. Phenylephrine- and high potassium-induced contractile responses were greater in NA than those in SHR aortic smooth muscle stripes. In NR, the contractile responses of high potassium (5.6$\times$10$\^$-2/ M) were not affected in the presence of GTS (300 $\mu$g/ml), PDS (300 $\mu$g/ml), and PTS (300 $\mu$g/ml), respectively whereas phenylephrine (10$\^$-6/ M)-induced contractile responses were markedly inhibited. In SHR, the contractile responses of high potassium (5.6$\times$10$\^$-2/ M) were not affected in the presence of GTS (300 $\mu$g/ml), PDS (300 $\mu$g/ml), and moderate doses of PTS (150-300 $\mu$g/ml), respectively but greatly blocked by high concentration of PTS (600 $\mu$g/ml). Phenylephrine (10$\^$-6/ M)-induced contractile responses were inhibited in a dose dependent fashion (150-600 $\mu$g/ml) by the pretreatment with PTS while not altered in the presence of GTS (300 $\mu$g/ml) and PDS (300 $\mu$g/ml), respectively. Taken together, these experimental results suggest that ginseng saponins cause vascular relaxation through blockade of adrenergic $\alpha$$\_$1/-receptors and some unknown mechanisms, and that there is some difference in sensitivity of vascular smooth muscle between NR and SHR in responses to ginseng saponins. It seems that panaxatriol type of some ginseng saponins has the greatest potency in vascular relaxation.

본 연구에서는 인삼사포닌 성분 즉, 총인삼사포닌(GTS), panaxadiol-type saponin(PDS) 및 panaxatriol-type saponin(PTS)이 정상 혈압쥐(NR) 및 자연발증 고혈압쥐(SHR)의 대동맥편에서 혈관수축약물의 수축반응에 대한 영향을 관찰하고자 시도하였으며, 얻어진 연구결과는 다음과 같다. Phenylephrine(아드레날린성 $\alpha$$_{-1}$-수용체 효능약)과 고농도 칼륨(막탈분극약)은 NR및 SHR의 대동맥편에서 각각 현저한 혈관수축반응을 나타내었다. 이들의 수축반응은 SHR보다 NR에서 현저하게 나타났다. NR에서 고농도 칼륨(5.6$\times$$10^{-2}$ M)에 의한 혈관수축반응은 GTS(300 $\mu$g/ml), PDS(300 $\mu$g/ml) 및 PTS(300 $\mu$g/ml)의 존재 하에서 각각 별다른 영향을 받지 않았다. 반면에, phenylephrine($10^{-6}$ M)에 의한 혈관수축반응은 현저하게 억제되었다. SHR에서 고농도 칼륨(5.6$\times$$10^{-2}$ M)에 의한 혈관수축반응은 GTS(300 $\mu$g/ml), PDS(300 $\mu$g/ml) 및 PTS(300 $\mu$g/ml)의 존재하에서 각각 별다른 영향을 받지 않았으나 고농도의 PTS(600 $\mu$g/ml)의 전처치에 의해서 유의하게 억제되었다. Phenylephrine($10^{-6}$ M)에 의한 혈관수축반응은 PTS의 전처치에 의해서 용량 의존적(150-600 $\mu$g/ml)으로 유의하게 억제되었으나 GTS(300 $\mu$g/ml)나 PDS(300 $\mu$g/ml)의 존재 하에서는 별다른 영향을 받지 않았다. 이상과 같은 실험 결과를 종합하여 보면, 인삼사포닌 성분은 흰쥐 적출 대동맥편에서 아드레날린성 $\alpha$$_{-1}$-아드레날린 수용체 차단작용과 일부 미지의 기전에 의해서 혈관이완작용을 일으키며, 이러한 인삼사포닌 성분에 대한 반응에서 NR과 SHR간에 혈관 평활근의 감수성의 차이가 있는 것으로 생각된다. 또한 인삼사포닌 성분 중 PTS가 혈관이완작용에 대한 효력이 가장 큰 것으로 사료된다.

Keywords

References

  1. Kim. N. D., Sang, S. Y and Schni-Ker th, V. B.: Gen. Pharmacol. 25, 1071 (1998)
  2. Kar.g, S. Y., Schni-Kerth, V.B. and Kim, N.D. : Life Sci. 56, 1564 (1995)
  3. Kim. N. D., Kang, S. Y., Kim, M. J., Park, J. H. and Kang, K. W. : Proceedings of the 7th International Symposium on Ginseng. Seoul, p.182 (1998)
  4. Jin, E. Y., Jin, M., Wei, Y. L., Huang, L. H., Yan, X. P., Shi, Z. X., Huang, L., Shen, D. C., Fu, R. J., Zhao, T.Y., Nam, K. Y. and Kumagai, A.: Proceedings of the 7th International Symposium on Ginseng. Seoul, p.190 (1998)
  5. Hong, S. P., Chi, H., Cho, S. H., Lee, Y. K., Woo, S. C., Kim, I. S., Oh, S. H., Yang, W. H. and Lim, D. Y. : Korean J. Hypert. 5(2), 159 (1999)
  6. Lim. D. Y., Park, K. B., Kim, K. H., Moon, J. K. and Kim, Y. H. : Korean Biochem. J. 20(3), 230 (1987)
  7. Lim , D. Y, Park, K. B., Kim, K. H., Choi, C. H., Bae, J. W. and Kim, M. W. : Korean J. Pharmacol. 24(1), 31 (1988)
  8. Lim , D. Y., Choi, C.H., Kim, C. D., Kim, K. H., Kim, S. B., Lee, B. J. and Chung, M. H. : Arch. Pharm. Res. 12(3), 166 (1989) https://doi.org/10.1007/BF02855549
  9. Lim, D. Y., Park, K. B., Kim, K. H., Moon, J. K., Lee, K. S., Kim, Y. K., Chung, Y. H. and Hong, S. P. : SOONHWANKI 17(3), 409 (1987)
  10. Hsu, S. T. : Jap. J. Pharmacol. 6, 18(1956) https://doi.org/10.1254/jjp.6.18
  11. Ozaki, J., Nakajima, T. and Takamori, T. : Fol. Pharmacol. Jap. 59, 27 (1963)
  12. Oh, J. S., Lim, J. K., Park, C. Wand Han, M. J. : Korean J. Pharmacol. 4,27 (1968)
  13. Lee, S. B. and Cho, K. C. : J. Cath. Med. Coll. 20, 89 (1971)
  14. Lee, K. S.: Proceedings of the 1st international Ginseng Symposium, Korea Ginseng Research Institute, Seoul, Korea p.57 (1974)
  15. Kitagawa, H. and Iwaki, R.: Fol. Pharmacol. Jap. 59(5), 345 (1963)
  16. Siegel, R. K. : J.A.M.A. 241, 1614 (1979) https://doi.org/10.1001/jama.241.15.1614
  17. Park, D. I. : Korean Med. J. 5, 18 (1960)
  18. Petkov, W. : Arznainmitte Forschung 11, 418 (1961)
  19. Watkins, R. W and Davidson, W.F.: European J. Pharmacol. 62, 191 (1980) https://doi.org/10.1016/0014-2999(80)90275-7
  20. Sohn, E. S., Park, S. C.,Huh, B. Y., Lee, C. K., Rhim, H. K., Ham, J. S., Yang, C. M., Han, C. S., Park, C. W. and Kim, H. J. : J. Korean Med. Assoc. 22(9), 731 (1979)
  21. Sohn, E. S., Park, S. C., Huh, B. Y., Lee, D. H., Rhim, H. K., Young, C. M., Han, C. S., Song, B. S. Kim, S. J., Park, C. W. and Kim, H. J. : J. Korea Med. Assoc. 23(1), 37-48(1980)
  22. Seok, S. E., Park, C. H., Nam, S. H., Choi, H. S., Lee, J. J., Lee, D. H., Huh, B. Y and Soh, E. S. : J Korean Med. Assoc. 24(6), 509 (1981)
  23. Sokabe, H., Kishi, K. and Watanabe, T. X. : Proceeding of the 4th international ginseng symposium, Korea Ginseng Research Institute, Seoul, p.57 (1984)
  24. Tallarida, R. J. and Murray, R. B. : Manual of pharmacologic calculations with computer programs. 2nd ed Springer-Verlag, New York, p.131 (1987)
  25. Wada, A., Takara, H., Izumi, F., Kobayashi, H. and Yanagihara, N. : Neuroscience 15, 283 (1985) https://doi.org/10.1016/0306-4522(85)90135-6
  26. Constantine, J. W., Mcshane, W. K., Scriabine, A. and Hess, H. J. : Hypertension: Mechanisms and Management, Grume & Stratton Inc. New York, p.429 (1973)
  27. Freis, E. E., Mackey, J. D. and Oliver, W. F.: Cir. Res. 3, 254 (1951) https://doi.org/10.1161/01.CIR.3.2.254
  28. Ablad, B., Borg, K. O., Carlsson, E., Johnsson, G., Malmfors, L. and Regardh, C. G. : Acta Pharmacol. Toxicol. 36, Suppl. V 7 (1975)
  29. Bolton, T. M. : Physiol. Rev. 3, 60(1979)
  30. Schwartz, A. and Taira, N. : Circ. Res. 52, 1(1983) https://doi.org/10.1161/01.RES.52.1.1
  31. Dube, G. P., Baik, Y. H. and Schwartz, A. : J. Cardiovasc. Pharmacol. 7, 377 (1985) https://doi.org/10.1097/00005344-198503000-00025
  32. Dube, G. P., Baik, Y. H., Van Breemen, C. and Schwartz, A. : European J. Pharmacol. 145, 39 (1988) https://doi.org/10.1016/0014-2999(88)90346-9
  33. Kim, J. M., Park, K. O. and Baik, Y. H. : Chonnam J. Med. Sci. 2(1), 50 (1989)
  34. Fleckenstein, A. : Ann. Rev. Pharmacol. Toxicol. 17, 149 (1977) https://doi.org/10.1146/annurev.pa.17.040177.001053
  35. Schwartz, A., Triggle, D. J. : Ann. Rev. Med. 35, 325(1984) https://doi.org/10.1146/annurev.me.35.020184.001545
  36. Wood, W. B., Roh, B. L. and White, R. P. : Jap. J. Pharmacol. 14(3), 284 (1964) https://doi.org/10.1254/jjp.14.284
  37. Imai, S., Kitagawa: Jap. J. Pharmacol. 31, 193(1981) https://doi.org/10.1254/jjp.31.193
  38. Ito, Y., Kitamura, K. and Kuriyama, H. : Br. J. Pharmacol. 7, 197 (1980)
  39. Ito, Y., Kitamura, K. and Kuriyama, H. : J. Physiol. 309, 171 (1980) https://doi.org/10.1113/jphysiol.1980.sp013502
  40. Bevan, J. A. : Am. J. Cardiol. 46, 519 (1982) https://doi.org/10.1016/S0002-9149(82)80005-2