Nitric oxide-dependent activation of pig oocytes: Role of calcium

Pig oocytes matured in vitro are parthenogenetically activated after treatment with nitric oxide (NO)-donor SNAP. The chelation of intracellular calcium ions with BAPTA-AM suppressed the SNAP-induced activation in a dose-dependent manner. Activation by a NO-donor is dependent on the influx of calciu...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2005-10, Vol.242 (1), p.16-22
Main Authors: Petr, Jaroslav, Rajmon, Radko, Lánská, Vilma, Sedmíková, Markéta, Jílek, František
Format: Article
Language:English
Subjects:
Animals
Calcium
Calcium - metabolism
Egtazic Acid - analogs & derivatives
Egtazic Acid - pharmacology
Female
Heparin - pharmacology
Macrocyclic Compounds
Nitric oxide
Nitric Oxide - metabolism
Oocyte
Oocytes - drug effects
Oocytes - metabolism
Oxazoles - pharmacology
Parthenogenetic activation
Pig
Procaine - pharmacology
Ruthenium Red - pharmacology
Swine
Verapamil - pharmacology
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Summary:Pig oocytes matured in vitro are parthenogenetically activated after treatment with nitric oxide (NO)-donor SNAP. The chelation of intracellular calcium ions with BAPTA-AM suppressed the SNAP-induced activation in a dose-dependent manner. Activation by a NO-donor is dependent on the influx of calcium from extracellular spaces, because the blockage of calcium channels by verapamil had significantly reduced the activation rate in SNAP-treated oocytes. The blockage of inositol triphosphate receptors had no effect on the activation of oocytes by a NO-donor. On the other hand, the blockers of ryanodine receptors, procaine and ruthenium red, inhibited the activation of oocytes induced by a NO-donor. These data indicate that the activation of pig oocytes by a NO-donor is calcium-dependent. The calcium for the activation is mobilized from extracellular and intracellular spaces. For the mobilization of intracellular calcium stores, it is the ryanodine receptors and not the inositol triphosphate receptors that play a key role.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2005.05.004