-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.
Pyanova et al. (2026) studied this question.