PROTEIN-KINASE-C PLAYS NO ROLE IN KCL-INDUCED VASCULAR CONTRACTION INCA2-FREE MEDIUM()

To examine the role of protein kinase C (PKC) on the sustained contrac tile responses of rat aorta to high KCI in isotonic Ca2+- and Mg2+-fre e solutions. METHODS: The effects of phorbol 12-myristate 13-acetate ( PMA, a PKC activator) and Calphostin C (a selective PKC inhibitor) wer e observed on the sustained contraction of rat aorta induced by K+ 136 mmol . L(-1). EGTA (100 mu mol . L(-1)) was added to prepare the Ca2-free medium and EDTA (100 mu mol . L(-1)) was added to reduce or remo ve the Mg2+. RESULTS: Aortic contraction to KCI was prominent in low M g2+ medium and was enhanced by EDTA (K-EDTA contraction). Such contrac tion was concentration dependently inhibited by Mg2+, but was not affe cted by Calphostin C 1 mu mol . L(-1). Pretreatment of the aortic prep arations with PMA (0.8 mu mol . L(-1)) potentiated the contraction to KCI in Ca2+-free, low Mg2+ medium and higher concentration of Mg2+ was required to cause relaxation. Such a reduced sensitivity to Mg2+ in t he presence of PMA was partially reversed by Calphostin C and was acco mpanied by an increased sensitivity to Ca2+, which concentration-depen dently caused contraction following Mg2+-induced relaxation. However, in the presence of EDTA 100 mu mol . L(-1) leg, Mg2+-free medium), the maximal contraction to KCI in Ca2+ free medium was not affected by PM A or Calphostin C. CONCLUSION: KCI-induced contraction in Ca2+-free an d Mg2+-free + EDTA 100 mmol . L(-1) medium was not affected by PMA or Calphostoin C. indicating that PKC plays no role in such contractile r esponses.