Magnesium ions but not ATP inhibit cyclic ADP-ribose-induced calcium release.
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.
Graeff
R M
RM
Department of Physiology, University of Minnesota, Minneapolis 55455.
Podein
R J
RJ
Aarhus
R
R
Lee
H C
HC
D000246:Adenosine Diphosphate Ribose / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D036563:Cyclic ADP-Ribose; D005260:Female; D007700:Kinetics; D015636:Magnesium Chloride / Q000494:pharmacology*; D009865:Oocytes / Q000187:drug effects / Q000378:metabolism*; D012617:Sea Urchins
D015636:Magnesium Chloride; D036563:Cyclic ADP-Ribose; D000246:Adenosine Diphosphate Ribose; D000255:Adenosine Triphosphate; D002118:Calcium