Magnesium ions but not ATP inhibit cyclic ADP-ribose-induced calcium release

Biochem Biophys Res Commun. 1995 Jan 17;206(2):786-91. doi: 10.1006/bbrc.1995.1111.


The pharmacology of the cyclic ADP-ribose (cADPR)-dependent Ca2+ release mechanism is very similar to that of the ryanodine receptor (RyR). Here we showed that MgCl2, a known inhibitor of RyR, blocked cADPR-induced Ca+2 release in sea urchin egg homogenates with a half maximal concentration of about 2.5 mM. The effect was specific since up to 10 mM Mg+2 had no effect on the Ca+2 release induced by inositol trisphosphate. K2ATP, another known modulator of RyR, at up to 10 mM did not affect the half-maximal concentration of cADPR, which remained at about 96 nM. These results indicate cADPR is a specific Ca+2 release activator and not merely an adenine nucleotide acting on the ATP-site. The inhibitory effects of Mg+2 further demonstrate the similarity between RyR and the cADPR-dependent Ca+2 release system.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenosine Diphosphate Ribose / analogs & derivatives*
  • Adenosine Diphosphate Ribose / antagonists & inhibitors
  • Adenosine Diphosphate Ribose / pharmacology
  • Adenosine Triphosphate / pharmacology*
  • Animals
  • Calcium / metabolism*
  • Cyclic ADP-Ribose
  • Female
  • Kinetics
  • Magnesium Chloride / pharmacology*
  • Oocytes / drug effects
  • Oocytes / metabolism*
  • Sea Urchins


  • Magnesium Chloride
  • Cyclic ADP-Ribose
  • Adenosine Diphosphate Ribose
  • Adenosine Triphosphate
  • Calcium