Planta Med 2002; 68(2): 133-137
DOI: 10.1055/s-2002-20259
Original Paper
Pharmacology
© Georg Thieme Verlag Stuttgart · New York

Involvement of Protein Kinase C and Na+/K+-ATPase in the Contractile Response Induced by Myricetin in Rat Isolated Aorta

Rosario Jiménez1 , Antonio Zarzuelo1 , Milagros Galisteo1 , Juan Duarte1
  • 1Department of Pharmacology, School of Pharmacy, University of Granada, Granada, Spain
Further Information

Publication History

February 12, 2001

June 30, 2001

Publication Date:
22 February 2002 (online)

Abstract

The role of PKC and Na+/K+-ATPase in the vascular smooth muscle responses induced by the bioflavonoid myricetin was investigated. KCl induced a concentration-dependent relaxation in arteries exposed to K+-free solution that was mainly mediated by an activation of Na+/K+-ATPase. Myricetin (50 μM) partially inhibited this vasorelaxant effect induced by KCl in intact rings, being unaffected in the endothelium-denuded rings. This inhibitory effect induced by myricetin was suppressed by the PGH2-TXA2 receptor antagonist, SQ 29,548, and the PKC inhibitor, staurosporine. Myricetin also induced an endothelium-dependent contractile response which was increased in the presence of PMA and reduced by staurosporine. In conclusion, myricetin both modulates Na+/K+-ATPase-induced vasodilatation acting as a functional inhibitor of Na+/K+-ATPase activity and activates protein kinases, including PKC, to induce contraction. These effects appear to be related to the activation of PGH2-TXA2 receptors on vascular smooth muscle by the TXA2 released from endothelium.

Abbreviations

NA:noradrenaline

NA+/K+-ATPase pump:sodium-potassium-activated ATPase

PKC:protein kinase C

PMA:phorbol 12-myristate 13-acetate

TXA2:thromboxane A2

Abstract

The role of PKC and Na+/K+-ATPase in the vascular smooth muscle responses induced by the bioflavonoid myricetin was investigated. KCl induced a concentration-dependent relaxation in arteries exposed to K+-free solution that was mainly mediated by an activation of Na+/K+-ATPase. Myricetin (50 μM) partially inhibited this vasorelaxant effect induced by KCl in intact rings, being unaffected in the endothelium-denuded rings. This inhibitory effect induced by myricetin was suppressed by the PGH2-TXA2 receptor antagonist, SQ 29,548, and the PKC inhibitor, staurosporine. Myricetin also induced an endothelium-dependent contractile response which was increased in the presence of PMA and reduced by staurosporine. In conclusion, myricetin both modulates Na+/K+-ATPase-induced vasodilatation acting as a functional inhibitor of Na+/K+-ATPase activity and activates protein kinases, including PKC, to induce contraction. These effects appear to be related to the activation of PGH2-TXA2 receptors on vascular smooth muscle by the TXA2 released from endothelium.

Abbreviations

NA:noradrenaline

NA+/K+-ATPase pump:sodium-potassium-activated ATPase

PKC:protein kinase C

PMA:phorbol 12-myristate 13-acetate

TXA2:thromboxane A2

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Prof. Dr. J. Duarte

Department of Pharmacology

School of Pharmacy

University of Granada

18071 Granada

Spain

Email: jmduarte@platon.ugr.es

Fax: +34-958-248964