Activation of protein kinase C attenuates the cyclic GMP responses to C-type natriuretic peptide in cultured mouse astrocytes

FEBS Lett. 1992 Aug 24;308(3):301-4. doi: 10.1016/0014-5793(92)81298-z.

Abstract

C-type natriuretic peptide (CNP), a recently discovered natriuretic peptide, has a potent stimulatory effect on cyclic GMP (cGMP) formation in cultured mouse astrocytes. Pretreatment of astrocytes with phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), attenuated CNP-induced cGMP responses in a dose-dependent manner, with a half-maximal inhibitory concentration of 6 nM, whereas the inactive phorbol ester analog, 4 alpha-phorbol 12,13-didecanoate, was without effect. In the presence of staurosporine, a PKC inhibitor, the inhibitory effect of PMA on CNP-stimulated cGMP production was reversed. These results suggest that PKC is an inhibitory modulator of CNP-stimulated cGMP responses in astrocytes and that CNP may interact with neuropeptides which stimulate PKC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects
  • Astrocytes / metabolism*
  • Atrial Natriuretic Factor / pharmacology*
  • Cells, Cultured
  • Cyclic GMP / metabolism*
  • Dose-Response Relationship, Drug
  • Enzyme Activation
  • Mice
  • Natriuretic Peptide, C-Type
  • Nerve Tissue Proteins / pharmacology*
  • Protein Kinase C / metabolism*
  • Tetradecanoylphorbol Acetate / analogs & derivatives
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Nerve Tissue Proteins
  • Natriuretic Peptide, C-Type
  • Atrial Natriuretic Factor
  • Protein Kinase C
  • Cyclic GMP
  • Tetradecanoylphorbol Acetate