蛋白激酶C不参与在无钙溶液内高钾引起的血管收缩

Protein kinase C plays no role in KCl induced vascular contraction =in Ca 2+ free medium

蛋白激酶Ｃ不参与在无钙溶液内高钾引起的血管收缩关超然２，ＧｅｎｎａｄｉＭＫＲＡＶＴＳＯＶ（ＤｅｐａｒｔｍｅｎｔｏｆＰｈｙｓｉｏｌｏｇｙ，ＦａｃｕｌｔｙｏｆＭｅｄｉｃｉｎｅ，ＴｈｅＵｎｉｖｅｒｓｉｔｙｏｆＨｏｎｇＫｏｎｇ，ＨｏｎｇＫｏｎｇ）关键词钙；蛋...

IM: To examine the role of protein kinase C (PKC) on the sustained contractile responses of rat aorta to high KCl in isotonic Ca 2+ and Mg 2+ free solutions. METHODS: The effects of phorbol 12 myristate 13 acetate (PMA, a PKC activator) and Calphostin C (a selective PKC inhibitor) were observed on the sustained contraction of rat aorta induced by K + 136 mmol·L -1 . EGTA (100 μmol ·L -1 ) was added to prepare the Ca 2+ free medium and EDTA (100 μmol·L -1 ) was added to reduce or remove the Mg 2+ . RESULTS: Aortic contraction to KCl was prominent in low Mg 2+ medium and was enhanced by EDTA (K EDTA contraction). Such contraction was concentration dependently inhibited by Mg 2+ , but was not affected by Calphostin C 1 μmol·L -1 . Pretreat￣ment of the aortic preparations with PMA (0 8 μmol·L -1 ) potentiated the contraction to KCl in Ca 2+ free, low Mg 2+ medium and higher concentration of Mg 2+ was required to cause relaxation. Such a reduced sensitivity to Mg 2+ in the presence of PMA was partially reversed by Calphostin C and was accompanied by an increased sensitivity to Ca 2+ , which concen￣tration dependently caused contraction following Mg 2+ induced relaxation. However, in the presence of EDTA 100 μmol·L -1 (eg, Mg 2+ free medium), the maximal contraction to KCl in Ca 2+ free medium was not affected by PMA or Calphostin C. CONCLUSION: KCl induced contraction in Ca 2+ free and Mg 2+ free+EDTA 100 mmol·L -1 medium was not affected by PMA or Calphostoin C, indicating that PKC plays no role in such contractile responses.