Supplementary Materials

Supplementary Materials for:

Pressure-induced oxidative activation of PKG enables vasoregulation by Ca2+ sparks and BK channels

Kaivan Khavandi, Rachael L. Baylie, Sarah A. Sugden, Majid Ahmed, Viktoria Csato, Philip Eaton, David C. Hill-Eubanks, Adrian D. Bonev, Mark T. Nelson, Adam S. Greenstein*

*Corresponding author. Email: adam.greenstein{at}manchester.ac.uk

This PDF file includes:

  • Fig. S1. Oxidant-activated PKG is required for BK channel activity to oppose pressure-induced constriction.
  • Fig. S2. Oxidative dimerization of PKG in arteries exposed to pressure and H2O2.
  • Fig. S3. Intraluminal pressure increases oxidant amounts in mesenteric arteries.
  • Fig. S4. H2O2 has no effect on K+ currents in the absence of Ca2+ sparks.
  • Fig. S5. Pharmacological manipulation of Ca2+ sparks.
  • Fig. S6. Caffeine-induced Ca2+ transients in wild-type and PKG[C42S]KI mesenteric arteries.
  • Fig. S7. Working model for the role of PKG and pressure-induced ROS.

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Citation: K. Khavandi, R. L. Baylie, S. A. Sugden, M. Ahmed, V. Csato, P. Eaton, D. C. Hill-Eubanks, A. D. Bonev, M. T. Nelson, A. S. Greenstein, Pressure-induced oxidative activation of PKG enables vasoregulation by Ca2+ sparks and BK channels. Sci. Signal. 9, ra100 (2016).

© 2016 American Association for the Advancement of Science