
Opening of glibenclamide-sensitive K+ channels in follicular cells promotes Xenopus oocyte maturation.
Author(s) -
Flemming Wibrand,
Eric Honoré,
Michel Lazdunski
Publication year - 1992
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.89.11.5133
Subject(s) - glibenclamide , oocyte , xenopus , pinacidil , medicine , endocrinology , follicular phase , hyperpolarization (physics) , chemistry , ovarian follicle , follicle , biology , microbiology and biotechnology , biochemistry , embryo , nuclear magnetic resonance spectroscopy , gene , diabetes mellitus , organic chemistry
The vasorelaxing K+ channel opener P1060 (a pinacidil analog), gonadotropins, and cAMP were shown to activate a glibenclamide-sensitive 86Rb+ efflux from fully grown follicle-enclosed Xenopus oocytes. Glibenclamide-sensitive K+ channels are located in follicular cells. Glibenclamide (i) depressed the gonadotropin- but not the progesterone-induced maturation and (ii) did not significantly modify progesterone production in oocytes exposed to Xenopus gonadotropin. In follicle-enclosed oocytes, the opener P1060 very significantly enhanced the oocyte sensitivity to progesterone. This increased sensitivity to the hormone induced by the K+ channel opener was reversed by glibenclamide. Thus these results suggest that the opening of glibenclamide-sensitive K+ channels in follicular cells by gonadotropins (and other activators of this channel) induces a hyperpolarization in the oocyte that greatly facilitates maturation by increasing the oocyte sensitivity to progesterone.