Thiol reagents increase the affinity of the inositol 1,4,5-trisphosphate receptor

Hilly, Mauricette; Piétri‐Rouxel, France; Coquil, Jean-François; Guy, Muriel; Mauger, Jean‐Pierre

doi:10.1016/s0021-9258(19)85446-7

Cited by 89 publications

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“…Finally the receptor activity is also regulated by intracellular Mg2+ (Vamey et al, 1990;Volpe et al, 1990), pH (Brass & Joseph, 1985;Guillemette & Segui, 1988;Joseph et al, 1989;Worley et al, 1987), and redox state (Bird et al, 1993;Bootmann et al, 1992;Poitras et al, 1993;Swann, 1991;Hilly et al, 1993).…”

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confidence: 99%

Bidirectional Activity of the Endoplasmic Reticulum Ca2+-ATPase of Bovine Adrenal Cortex

Poitras¹,

Ribeiro-Do-Valle²,

Poirier³

et al. 1995

Biochemistry

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It is generally accepted that the ryanodine receptor and the inositol 1,4,5-trisphosphate receptor play major roles in the complex mechanisms by which agonists increase intracellular Ca2+ concentration. In these mechanisms, the endoplasmic reticulum Ca(2+)-ATPase has been attributed an accessory role of refilling the intracellular Ca2+ store. In the present study, the activity of the microsomal Ca(2+)-ATPase of bovine adrenal cortex was investigated. We show that the Ca(2+)-pumping activity of the Ca(2+)-ATPase is related to the ADP/ATP ratio. Our results also show that a brisk increase of the ADP/ATP ratio upon addition of exogenous ADP triggered a rapid release of Ca2+ from preloaded microsomes. ADP released Ca2+ in a dose-dependent manner with an EC50 of 2.98 +/- 0.78 mM. ADP-induced Ca2+ release was not prevented by heparin, ruling out the participation of the inositol 1,4,5-trisphosphate receptor. ADP-induced Ca2+ release could not be attributed to the mere inhibition of the Ca(2+)-ATPase, since the rate of ADP-induced Ca2+ release was 20 times faster than the rate of Ca2+ release induced by a maximal concentration of thapsigargin (2 microM). ADP-induced Ca2+ release experiments performed in the presence of [32P]PO4 revealed a concomitant production of [32P]ATP. ADP-induced [32P]ATP production was dose-dependent, with an EC50 of 5.50 +/- 0.70 mM. ADP-induced [32P]ATP production was prevented by ionomycin (10 microM) and by high concentrations of extramicrosomal Ca2+. These results demonstrate that the microsomal Ca(2+)-ATPase of adrenal cortex possesses a bidirectional activity that depends on ADP concentrations, the Ca2+ gradient across the microsomal membrane, and probably also ATP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

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