Dihydropyridines, known for blocking L-type calcium channels, also interact with the open state of Shaker K+ channels to induce voltage-dependent inactivation.
DHPs may exert off-target effects on K+ channels; leaves open physiological relevance in native mammalian systems.
Dihydropyridines (DHPs) are well known for their effects on L-typed voltage-dependent Ca2+ channels, However, these drugs also affect other voltage-dependent ion channels, including Shaker K+ channels. We examined the effects of DHPs on the Shaker K+ channels expressed in Xenopus oocytes. Intracellular applications of DHPs quickly and reversibly induced apparent inactivation in the Shaker K+ mutant channels with disrupted N- and C-type inactivation. We found that DHPs interact with the open state of the channel as evidenced by the decreased mean open time. The DHPs effects are voltage-dependent, becoming more effective with hyperpolarization. A model which involves binding of two DHP molecules to the channel is consistent with the results obtained in our experiments.
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Avdonin et al. (1997) studied this question.
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