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May 14, 2026The FASEB Journal1 citationsOpen Access

Orchestration of PKC ‐Mediated Inhibition and Calcium Release‐Mediated Activation of BK Currents in Rat Vascular Smooth Muscle Cells by Melatonin Confers a BK ‐Channel‐Dependent Restraint on Melatonin‐Induced Vasocontraction

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APAnastasia PyanovaUniversity of AugsburgVKVjatscheslav U. KalentchukMoscow State University of Environmental EngineeringVSV. N. SerebryakovInstitute of Experimental Cardiology

Key Points

  • This research aims to explore how melatonin influences BK channel activity and vascular smooth muscle contraction.
  • Utilized calphostin C to inhibit PKC and assess its effects on BK currents in rat vascular smooth muscle cells.
  • Investigated the impact of TEA and iberiotoxin on melatonin-induced contraction in intact vessel preparations.
  • Examined signaling pathways involved in melatonin's action on vascular smooth muscle.
  • Calphostin C significantly increased BK current in the presence of melatonin.
  • Melatonin induced vasocontraction was enhanced by pre-treatment with TEA or iberiotoxin.
  • BK channels were identified as a critical target in melatonin signaling, highlighting PLC-dependent signaling interactions.

Abstract

-induced calcium release. Calphostin C, a specific PKC-inhibitor, further stimulated the BK current in the presence of melatonin, suggesting functional cross-talk between distinct PLC-dependent signaling branches. At the functional level, melatonin reversibly contracted intact vessel preparations. Vessel pre-treatment with TEA or iberiotoxin augmented the effect of melatonin. Together, these findings identify BK channels as a key downstream target of melatonin signaling in vascular smooth muscle and reveal a previously unrecognized PLC-dependent signaling cross-talk that contributes to melatonin-induced vasocontraction.

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Cite This Study

Pyanova et al. (2026) studied this question.

synapsesocial.com/papers/6a0566bda550a87e60a1eaadhttps://doi.org/10.1096/fj.202601214r
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