These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The effect of PI3 kinase inhibitor LY294002 on voltage-dependent K(+) channels in rabbit coronary arterial smooth muscle cells.
    Author: Hong DH, Choi IW, Son YK, Kim DJ, Na SH, Jung WK, Yoon YW, Park WS.
    Journal: Life Sci; 2013 May 20; 92(17-19):916-22. PubMed ID: 23557854.
    Abstract:
    AIMS: We examined the effect of LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, on voltage-dependent K(+) (Kv) channels. MAIN METHODS: Electrophysiological recordings were performed in freshly isolated rabbit coronary arterial smooth muscle cells. KEY FINDINGS: The Kv current amplitude was inhibited by LY294002 in a dose-dependent manner, with a Kd value of 1.48μM. Without alteration of the kinetics of activation, LY294002 accelerated the decay rate of Kv channel inactivation. The rate constants of association and dissociation for LY294002 were 1.83±0.01μM(-1)s(-1) and 2.59±0.14s(-1), respectively. Application of LY294002 had no significant impact on the steady-state activation or inactivation curves. In the presence of LY294002, the recovery time constant from inactivation was increased, and Kv channel inhibition increased under train pulses (1 or 2Hz). This indicates that LY294002-induced Kv channel inhibition is use-dependent. Furthermore, pretreatment with another PI3K inhibitor, wortmannin (10μM), did not affect the Kv current, and did not change the inhibitory effect of LY294002. SIGNIFICANCE: Based on these results, we suggest that LY294002 directly blocks Kv current irrespective of PI3K inhibition.
    [Abstract] [Full Text] [Related] [New Search]