Archives of Pharmacal Research

The Pharmaceutical Society of Korea (대한약학회)
권호 표지

Phorbol Ester-induced Contraction Through p38 Mitogen-activated Protein Kinase is Diminished in Aortas from DOCA-Salt Hypertensive Rats

  • Lee, Chang-Kwon (Department of Physiology, College of Medicine, Konkuk University) ;
  • Kim, Jung-Kwan (Department of Physical Therapy, College of Natural Science, Yongin University) ;
  • Won, Kyung-Jong (Department of Physiology, College of Medicine, Konkuk University) ;
  • Lee, Hwan-Myung (Department of Physiology, College of Medicine, Konkuk University) ;
  • Kim, Hyo-Jin (Department of Physiology, College of Medicine, Konkuk University) ;
  • Roh, Hui-Yul (Department of Physiology, College of Medicine, Konkuk University) ;
  • Park, Hyo-Jun (Department of Physiology, College of Medicine, Konkuk University) ;
  • Shin, Hwa-Sup (Division of Life Science, College of Biomedical and Health Science, Konkuk University) ;
  • Park, Tae-Kyu (Division of Life Science, College of Biomedical and Health Science, Konkuk University) ;
  • Kim, Bo-Kyung (Department of Physiology, College of Medicine, Konkuk University) ;
  • Lee, Sang-Mok (Department of Veterinary Physiology, College of Veterinary Medicine, Konkuk University)
  • Published : 2006.11.30
Download PDF
⟨ Previous Next ⟩

Abstract

The role of mitogen-activated protein kinase (MAPK) in the decreased contractile response to phorbol ester in aortic smooth muscle strips from deoxycorticosterone acetate (DOCA)-salt hypertensive rats was examined. Norepinephrine (NE) evoked greater contractility in aortic strips from DOCA rats than in those of sham-operated rats. 12-Deoxyphorbol 13-isobutyrate (DPB) induced contraction in $Ca^{2+}-free$ medium, which was diminished in strips from DOCA rats compared to sham-operated rats. Vasoconstrictions induced by these stimulants were inhibited by SB203580 and PD098059, inhibitors of p38 MAPK and extracellular signal-regulated kinase (ERK) 1/2, respectively, in both strips. The phosphorylation of p38 MAPK and ERK1/2 induced by NE was greater in strips from DOCA rats compared to those from sham-operated rats, and this phosphorylation was inhibited by the kinase inhibitors. DPB increased the phosphorylation of p38 MAPK and ERK1/2 in strips from both animals, and the increment of p38 MAPK phosphorylation by the stimulant was diminished in strips from DOCA rats compared to sham-operated rats. These findings suggest that the $Ca^{2+}-independent$ contraction evoked by DPB results from the activation of MAPKs in rat aortic smooth muscle and that the attenuated contractility by DPB in DOCA rat appears to be associated with diminished p38 MAPK activity.

Keywords

References

  1. Cain, A.E. and Khalil, R.A., Pathophysiology of essential hypertension: role of the pump, the vessel, and the kidney. Semin. Nephrol., 22, 3-16 (2002)
  2. Dessy, C., Kim, I., Sougnez, C.L., Laporte, R., and Morgan, K.G., A role for MAP kinase in differentiated smooth muscle contraction evoked by adrenoceptor stimulation. Am. J. Physiol., 275, C1081-C1086 (1998) https://doi.org/10.1152/ajpcell.1998.275.4.C1081
  3. Fu, X., Gong, M.C., Jia, T., Somlyo, A.V., and Somlyo, A.P., The effects of the Rho-kinase inhibitor Y-27632 on arachidonic acid-, GTPãS-, and phorbol ester-induced $Ca^{2+}$-sensitization of smooth muscle. FEBS Lett., 440, 183-187 (1998) https://doi.org/10.1016/S0014-5793(98)01455-0
  4. Hori, M., Sato, K., Sakata, K., Ozaki, H., Takano-Ohmuro, H., Tsuchiya, T., Sugi, H., Kato, I., and Karaki, H., Receptor agonists induce myosin phosphorylation-dependent and phosphorylation-independent contractions in vascular smooth muscle. J. Pharmacol. Exp. Ther., 261, 506-512 (1992)
  5. Horowitz, A., Clement-Chomienne, O., Walsh, M.P., and Morgan, K.G., Epsilon-isoenzyme of protein kinase C induces a $Ca^{2+}$-independent contraction in vascular smooth muscle. Am. J. Physiol., 271, C589-C594 (1996) https://doi.org/10.1152/ajpcell.1996.271.2.C589
  6. Kamm, K.E. and Stull, J.T., The function of myosin and myosin light chain kinase phosphorylation in smooth muscle. Annu. Rev. Pharmacol. Toxicol., 25, 593-620 (1985) https://doi.org/10.1146/annurev.pa.25.040185.003113
  7. Kamp, T.J. and Hell, J.W., Regulation of cardiac L-type calcium channels by protein kinase A and protein kinase C. Circ. Res., 87, 1095-102 (2000) https://doi.org/10.1161/01.RES.87.12.1095
  8. Karaki, H., Ozaki, H., Hori, M., Mitsui-Saito, M., Amano, K., Harada, K., Miyamoto, S., Nakazawa, H., Won, K.J., and Sato, K., Calcium movements, distribution, and functions in smooth muscle. Pharmacol. Rev., 49, 157-230 (1997)
  9. Khalil, R.A., Lajoie, C., Resnick, M.S., and Morgan, K.G., $Ca^{2+}$-independent isoforms of protein kinase C differentially translocate in smooth muscle. Am. J. Physiol., 263, C714- C719 (1992) https://doi.org/10.1152/ajpcell.1992.263.3.C714
  10. Khalil, R.A. and Morgan, K.G., PKC-mediated redistribution of mitogen-activated protein kinase during smooth muscle cell activation. Am. J. Physiol., 265, C406-C411 (1993) https://doi.org/10.1152/ajpcell.1993.265.2.C406
  11. Kim, B., Kim, Y.S., Ahn, J., Kim, J., Cho, S.I., Won, K.J., Ozaki, H., Karaki, H., and Lee, S., Conventional-type protein kinase C contributes to phorbol ester-induced inhibition of rat myometrial tension. Br. J. Pharmacol., 139, 408-414 (2003b) https://doi.org/10.1038/sj.bjp.0705237
  12. Kim, B., Kim, J., Bae, Y.M., Cho, S.I., Kwon, S.C., Jung, J.Y., Park, J.C., and Ahn, H.Y., p38 Mitogen-activated protein kinase contributes to the diminished aortic contraction by endothelin-1 in DOCA-salt hypertensive rats. Hypertension, 43, 1086-1091 (2004a) https://doi.org/10.1161/01.HYP.0000125995.85427.fd
  13. Kim, Y.S., Kim, B., Karaki, H., Hori, M., and Ozaki, H., Upregulation of Rnd1 during pregnancy serves as a negativefeedback control for $Ca^{2+}$ sensitivity of contractile elements in rat myometrium. Biochem. Biophys. Res. Commun., 311, 972-978 (2003a) https://doi.org/10.1016/j.bbrc.2003.10.100
  14. Kim, B., Kim, J., Kim, A., Kim, Y.S., Lee, Y.R., Bae, Y.M., Cho, S., and Ryu, M.R., Ligusticum wallichi-induced vasorelaxation mediated by mitogen-activated protein kinase in rat aortic smooth muscle. J. Ethnopharmacol., 90, 397-401 (2004b) https://doi.org/10.1016/j.jep.2003.11.003
  15. Kim, J., Lee, Y.R., Lee, C.H., Choi, W.H., Lee, C.K., Kim, J., Bae, Y.M., Cho, S., and Kim, B., Mitogen-activated protein kinase contributes to elevated basal tone in aortic smooth muscle from hypertensive rats. Eur. J. Pharmacol., 514, 209- 215 (2005) https://doi.org/10.1016/j.ejphar.2005.03.030
  16. Kitazawa, T., Eto, M., Woodsome, T.P., and Brautigan, D.L., Agonists trigger G protein-mediated activation of the CPI-17 inhibitor phosphoprotein of myosin light chain phosphatase to enhance vascular smooth muscle contractility. J. Biol. Chem., 275, 9897-9900 (2000) https://doi.org/10.1074/jbc.275.14.9897
  17. Kobayashi, N., Mita, S., Yoshida, K., Honda, T., Kobayashi, T., Hara, K., Nakanou, S., Tsubokou, Y., and Matsuoka, H., Celiprorol activates eNOS through the PI3K-Act pathway and inhibits VCAM-1 via NF-eB induced by oxidative stress. Hypertension, 42: 1004-1013 (2003) https://doi.org/10.1161/01.HYP.0000097547.35570.70
  18. Kwon, S., Lee, W.J., Fang, L.H., Kim, B., and Ahn, H.Y., Mitogen-activated protein kinases partially regulate endothelin-1-induced contractions through a myosin light chain phosphorylation-independent pathway. J. Vet. Med. Sci., 65, 225-230 (2003) https://doi.org/10.1292/jvms.65.225
  19. Kwon, S., Fang, L.H., Kim, B., Ha, T.S., Lee, S.J., and Ahn, H.Y., p38 Mitogen-activated protein kinase regulates vasoconstriction in spontaneously hypertensive rats. J. Pharmacol. Sci., 95, 267-272 (2004) https://doi.org/10.1254/jphs.FPJ03091X
  20. Lee, Y.H., Kim, I., Laporte, R., Walsh, M.P., and Morgan, K.G., Isozyme-specific inhibitors of protein kinase C translocation: effects on contractility single permeabilized vascular muscle cells of the ferret. J. Physiol., 517, 709-720 (1999) https://doi.org/10.1111/j.1469-7793.1999.0709s.x
  21. Lee, Y.R., Lee, C.K., Park, H.J., Kim, H., Kim, J., Kim, J., Lee, K.S., Lee, Y.L., Min, K.O., and Kim, B., c-Jun N-terminal kinase contributes to norepinephrine-induced contraction through phosphorylation of caldesmon in rat aortic smooth muscle. J. Pharmacol. Sci., 100, 119-125 (2006) https://doi.org/10.1254/jphs.FP0050777
  22. Li, L., Eto, M., Lee, M.R., Morita, F., Yazawa, M., and Kitazawa, T., Possible involvement of the novel CPI-17 protein in protein kinase C signal transduction of rabbit arterial smooth muscle. J. Physiol., 508, 871-881 (1998) https://doi.org/10.1111/j.1469-7793.1998.871bp.x
  23. Liao, D.F., Monia, B., Dean, N., and Berk, B.C., Protein kinase C- mediates angiotensin II activation of ERK1/2 in vascular smooth muscle cells. J. Biol. Chem., 272, 6146-6150 (1997) https://doi.org/10.1074/jbc.272.10.6146
  24. McNair, L.L., Salamanca, D.A., and Khalil, R.A., Endothelin-1 promotes $Ca^{2+}$ antagonist-insensitive coronary smooth muscle contraction via activation of å-protein kinase C. Hypertension, 43, 897-904 (2004) https://doi.org/10.1161/01.HYP.0000118520.92686.3b
  25. Miyata, Y. and Nishida, E., Distantly related cousins of MAP kinase: biochemical properties and possible physiological functions. Biochem. Biophys. Res. Commun., 266, 291-295 (1999) https://doi.org/10.1006/bbrc.1999.1705
  26. Multhalif, M.M., Benter, I.F., Khandekar, Z., Gaber, L., Estes, A., Malik, S., Parmentier, J.H., Manne, V., and Malik, K.U., Contribution of Ras GTPase/MAP kinase and cytochrome P450 metabolites to deoxycorticosterone-salt induced hypertension. Hypertension, 35, 457-463 (2000) https://doi.org/10.1161/01.HYP.35.1.457
  27. Nixon, G.F., Iizuka, K., Haystead, C.M., Haystead, T.A., Somlyo, A.P., and Somlyo, A.V., Phosphorylation of caldesmon by mitogen-activated protein kinase with no effect on $Ca^{2+}$ sensitivity I rabbit smooth muscle. J. Physiol., 487, 283-289 (1995) https://doi.org/10.1113/jphysiol.1995.sp020879
  28. Park, S., Kim, B., Kim, J., Won, K.J., Lee, S., Kwon, S., and Cho, S., Tamoxifen induces vasorelaxation via inhibition of mitogen-activated protein kinase in rat aortic smooth muscle. J. Vet. Med. Sci., 65, 1155-1160 (2003) https://doi.org/10.1292/jvms.65.1155
  29. Sakamoto, K., Hori, M., Izumi, M., Oka, T., Kohama, K., Ozaki, H., and Karaki, H., Inhibition of high $K^+$-induced contraction by the ROCKs inhibitor Y-27632 in vascular smooth muscle: possible involvement of ROCKs in a signal transduction pathway. J. Pharmacol. Sci., 92, 56-69 (2003) https://doi.org/10.1254/jphs.92.56
  30. Sirous, Z.N., Fleming, J.B., and Khalil, R.A., Endothelin-1 enhances eicosanoids-induced coronary smooth muscle contraction by activating specific protein kinase C isoforms. Hypertension, 37, 497-504 (2001) https://doi.org/10.1161/01.HYP.37.2.497
  31. Taggart, M.J., Lee, Y.H., and Morgan, K.G. Cellular redistribution of PKC, rhoA, and ROK following smooth muscle agonist stimulation. Exp. Cell. Res., 25, 92-101 (1999)
  32. Tostes, R.C., David, F.L., Carvalho, M.H., Nigro, D., Scivoletto, R., and Fortes, Z.B., Gender differences in vascular reactivity to endothelin-1 in deoxycorticosterone-salt hypertensive rats. J. Cardiovasc. Pharmacol., 36, S99-S101 (2000) https://doi.org/10.1097/00005344-200036001-00032
  33. Touyz, R.M., El Mabrouk, M., He, G., Wu, X.H., and Schiffrin, E.L., Mitogen-activated protein/extracellular signal-regulated kinase inhibition attenuates angiotensin II-mediated signaling and contraction in spontaneously hypertensive rat vascular smooth muscle cells. Circ. Res., 84, 505-515 (1999) https://doi.org/10.1161/01.RES.84.5.505
  34. Walsh, M.P., Horowitz, A., Clement-Chomienne, O., Andrea, J.E., Allen, B.G., and Morgan KG., Protein kinase C mediation of $Ca^{2+}$-independent contractions of vascular smooth muscle. Biochem. Cell Biol., 74, 485-502 (1996) https://doi.org/10.1139/o96-053
  35. Watts, S.W., The development of enhanced arterial serotonergic hyper-responsiveness in mineralocorticoid hypertension. J. Hypertens., 16, 811-822 (1998) https://doi.org/10.1097/00004872-199816060-00012
  36. Widmann, C., Gibson, S., Jarpe, M.B., and Johnson, G.L., Mitogen-activated protein kinase: conservation of a threekinase module from yeast to human. Physiol. Rev., 79, 143- 180 (1999) https://doi.org/10.1152/physrev.1999.79.1.143