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Abstract
BK channels regulate vascular tone by hyperpolarizing smooth muscle in response to fluctuating calcium concentrations. Oestrogen has been reported to lower blood pressure by increasing BK channel open probability through direct binding to the regulatory β1-subunit(s) associated with the channel. The present investigation demonstrates that 17β-oestradiol activates the BK channel complex by increasing the burst duration of channel openings. A subconductance state was observed in 25% of recordings following the addition of 17β-oestradiol and could reflect uncoupling between the pore forming α1-subunit and the regulatory β1-subunit. We also present evidence that more than one β1-subunit is required to facilitate binding of 17β-oestradiol to the channel complex.
| Acronyms | ||
| BK channel | = | large conductance, Ca2+ and voltage dependent K+ channel |
| VDCC | = | Voltage dependent Ca2+ channels |
| STOC | = | spontaneous transient outward currents |
| Acronyms | ||
| BK channel | = | large conductance, Ca2+ and voltage dependent K+ channel |
| VDCC | = | Voltage dependent Ca2+ channels |
| STOC | = | spontaneous transient outward currents |