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  • Title: Electrophysiological and pharmacological characterization of the K(ATP) channel involved in the K+-current responses to FSH and adenosine in the follicular cells of Xenopus oocyte.
    Author: Fujita R, Kimura S, Kawasaki S, Watanabe S, Watanabe N, Hirano H, Matsumoto M, Sasaki K.
    Journal: J Physiol Sci; 2007 Feb; 57(1):51-61. PubMed ID: 17239259.
    Abstract:
    The follicular cells surrounding Xenopus oocyte under voltage clamp produce K(+)-current responses to follicle-stimulating hormone (FSH), adenosine (Ade), and intracellularly applied cAMP. We previously reported that these responses are suppressed by the stimulation of P2Y receptor through phosphorylation by PKC presumably of the ATP-sensitive K(+) (K(ATP)) channel. This channel comprises sulfonylurea receptors (SURs) and K(+) ionophores (Kirs) having differential sensitivities to K(+) channel openers (KCOs) depending on the SURs. To characterize the K(+) channels involved in the FSH- and Ade-induced responses, we investigated the effects of various KCOs and SUR blockers on the agonist-induced responses. The applications of PCO400, cromakalim (Cro), and pinacidil, but not diazoxide, produced K(+)-current responses similar to the FSH- and Ade-induced responses in the magnitude order of PCO400 > Cro >> pinacidil in favor of SUR2A. The application of glibenclamide, phentolamine, and tolbutamide suppressed all the K(+)-current responses to FSH, Ade, cAMP, and KCOs. Furthermore, both the FSH- and Ade-induced responses were markedly augmented during the KCO-induced responses, or vice versa. The I-V curves for the K(+)-current responses induced by Cro, Ade, and FSH showed outward rectification in normal [K(+)](o), but weak inward rectification in 122 mM [K(+)](o). Also, stimulations of P2Y receptor by UTP or PKC by PDBu markedly depressed the K(+)-current response to KCOs in favor of Kir6.1, as previously observed with the responses to FSH and Ade. These results suggest that the K(+)-current responses to FSH and Ade may be produced by the opening of a novel type of K(ATP) channel comprising SUR2A and Kir6.1.
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