Diabetes Upregulates BK(Ca) Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain.
V, S., I, I., D, D., M, M., O, B., & A, S. (2026). Diabetes Upregulates BK(Ca) Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain.. Microcirculation (New York, N.Y. : 1994). https://doi.org/10.1111/micc.70077
V S, I I, D D, M M, O B, A S. Diabetes Upregulates BK(Ca) Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain.. Microcirculation (New York, N.Y. : 1994). 2026; doi: 10.1111/micc.70077
V S, I I, D D, et al. Diabetes Upregulates BK(Ca) Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain.[J]. Microcirculation (New York, N.Y. : 1994). 2026. DOI: 10.1111/micc.70077.
@article{v2026,
author = {Sydorenko V and Ivanova I and Dryn D and Melnyk M and Boldyriev O and Soloviev A},
title = {Diabetes Upregulates BK(Ca) Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain.},
journal = {Microcirculation (New York, N.Y. : 1994)},
year = {2026},
doi = {10.1111/micc.70077},
note = {PMID: 42365666},
}
TY - JOUR AU - Sydorenko V AU - Ivanova I AU - Dryn D AU - Melnyk M AU - Boldyriev O AU - Soloviev A TI - Diabetes Upregulates BK(Ca) Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain. T2 - Microcirculation (New York, N.Y. : 1994) PY - 2026 DO - 10.1111/micc.70077 AN - PMID:42365666 ER -
OBJECTIVE: Large conductance calcium-activated potassium channels (BKCa) play an important role in the regulation of vascular tone. However, the properties of BKCa channels in smooth muscle of pulmonary arteries are poorly understood. Previous experimental studies demonstrated that pulmonary hypoxic vasoconstriction as a normal physiological response to decreased oxygen levels was impaired in diabetic animals due to abnormal activation of BKCa channels. The aim of this study was to identify mechanisms of diabetes-induced activation of BKCa channels in freshly isolated smooth muscle cells from rat pulmonary arteries. METHODS: Type 1 diabetes was induced by streptozotocin (STZ). Whole-cell potassium currents were recorded using the patch-clamp method. Expression levels of BK-α and BK-β1 subunits were measured by real-time PCR. RESULTS: Our results demonstrate that the amplitude of whole-cell current through BKCa channels in rat pulmonary artery smooth muscle cells is significantly increased during STZ-induced diabetes without altering the expression of BK-α and BK-β1 subunits and channel calcium sensitivity. The slow component of BKCa current deactivation time constant and spontaneous transient outward current amplitude were increased in diabetic animals compared to healthy animals. CONCLUSIONS: We conclude that abnormal activation of the BKCa channel in pulmonary arterial smooth muscle during diabetes is associated with alterations in the local control mechanism of the BKCa pore-gate domain.