scholarly journals Bisphenol A alters the function and expression of BK channels in vascular smooth muscle through membrane and nuclear signals

2012 ◽  
Author(s):  
Shinichi Asano
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Bisphenol A ◽  
Bk Channels

scholarly journals The Functional Availability of Arterial Kv7 Channels Is Suppressed Considerably by Large-Conductance Calcium-Activated Potassium Channels in 2- to 3-Month Old but Not in 10- to 15-Day Old Rats

2020 ◽  
Vol 11 ◽  
Author(s):  
Dongyu Ma ◽  
Dina Gaynullina ◽  
Nadine Schmidt ◽  
Mitko Mladenov ◽  
Rudolf Schubert
Keyword(s):  
Smooth Muscle ◽  
Potassium Channels ◽  
Vascular Smooth Muscle ◽  
Bk Channels ◽  
Similar Degree ◽  
Functional Impact ◽  
Adult Rat ◽  
Kv7 Channels ◽  
Contractile Effect ◽  
Arterial Contractility

BackgroundVoltage-gated potassium (Kv) channels, especially Kv7 channels, are major potassium channels identified in vascular smooth muscle cells with a great, albeit differential functional impact in various vessels. Vascular smooth muscle Kv7 channels always coexist with other K channels, in particular with BK channels. BK channels differ in the extent to which they influence vascular contractility. Whether this difference also causes the variability in the functional impact of Kv7 channels is unknown. Therefore, this study addressed the hypothesis that the functional impact of Kv7 channels depends on BK channels.Experimental ApproachExperiments were performed on young and adult rat gracilis and saphenous arteries using real-time PCR as well as pressure and wire myography.Key ResultsSeveral subfamily members of Kv7 (KCNQ) and BK channels were expressed in saphenous and gracilis arteries: the highest expression was observed for BKα, BKβ1 and KCNQ4. Arterial contractility was assessed with methoxamine-induced contractions and pressure-induced myogenic responses. In vessels of adult rats, inhibition of Kv7 channels or BK channels by XE991 or IBTX, respectively enhanced arterial contractility to a similar degree, whereas activation of Kv7 channels or BK channels by retigabine or NS19504, respectively reduced arterial contractility to a similar degree. Further, IBTX increased both the contractile effect of XE991 and the anticontractile effect of retigabine, whereas NS19504 reduced the effect of retigabine and impaired the effect of XE991. In vessels of young rats, inhibition of Kv7 channels by XE991 enhanced arterial contractility much stronger than inhibition of BK channels by IBTX, whereas activation of Kv7 by retigabine reduced arterial contractility to a greater extent than activation of BK channels by NS19504. Further, IBTX increased the anticontractile effect of retigabine but not the contractile effect of XE991, whereas NS19504 reduced the effect of retigabine and impaired the effect of XE991.ConclusionKv7 and BK channels are expressed in young and adult rat arteries and function as negative feedback modulators in the regulation of contractility of these arteries. Importantly, BK channels govern the extent of functional impact of Kv7 channels. This effect depends on the relationship between the functional activities of BK and Kv7 channels.

A human calcium-activated potassium channel gene expressed in vascular smooth muscle

1995 ◽  
Vol 269 (3) ◽  
pp. H767-H777 ◽  
Author(s):  
D. P. McCobb ◽  
N. L. Fowler ◽  
T. Featherstone ◽  
C. J. Lingle ◽  
M. Saito ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Splice Variants ◽  
Chinese Hamster Ovary Cells ◽  
Genomic Structure ◽  
Single Gene ◽  
Chinese Hamster ◽  
Bk Channels ◽  
Bk Channel ◽  
Amino Terminal

Large-conductance Ca(2+)-activated K+ (BK) channels are widespread and functionally heterogeneous. In other classes of K+ channels, functional heterogeneity derives from large gene families, alternative splicing, heterologous subunit composition, and functional modulation. The molecular basis of mammalian BK channel heterogeneity is unknown, since only a single gene (mSlo) has been identified. BK channels in native vascular smooth muscle have an apparent Ca2+ sensitivity approximately 10-fold greater than native brain or skeletal muscle channels, or cloned mSlo channels. Using mSlo as a low-stringency probe, we screened human arterial smooth muscle and genomic libraries extensively in search of genes or splice variants with novel properties. We isolated the human homologue of mSlo, including two novel splice variant forms, but found no other related genes. Electrophysiological characterization of the hSlo clones in Xenopus oocytes and Chinese hamster ovary cells gave BK currents that were not measurably different from mSlo currents. However, coexpression of hSlo with a recently cloned beta-subunit derived from smooth muscle dramatically increased apparent Ca2+ sensitivity. Thus alpha-subunits alone may not determine Ca2+ sensitivity of vascular smooth muscle BK channels. hSlo was mapped to human chromosome 10q23.1, and the genomic structure was analyzed. Immediately after the amino terminal, two unusual regions of trinucleotide repeating sequences are present. The first of these regions encodes polyglycine, and the second encodes polyserine. Both regions of repeated sequence are conserved between the mouse and human genome.

Activating BK channels ameliorates vascular smooth muscle calcification through Akt signaling

2021 ◽  
Author(s):  
Feng-ling Ning ◽  
Jie Tao ◽  
Dan-dan Li ◽  
Lu-lu Tian ◽  
Meng-ling Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Akt Signaling ◽  
Bk Channels

scholarly journals Calcium- and voltage-gated BK channels in vascular smooth muscle

2018 ◽  
Vol 470 (9) ◽  
pp. 1271-1289 ◽  
Author(s):  
Alex M. Dopico ◽  
Anna N. Bukiya ◽  
Jonathan H. Jaggar
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Bk Channels ◽  
Voltage Gated

scholarly journals βENaC is required for whole cell mechanically gated currents in renal vascular smooth muscle cells

2013 ◽  
Vol 304 (12) ◽  
pp. F1428-F1437 ◽  
Author(s):  
Wen-Shuo Chung ◽  
Jennifer L. Weissman ◽  
Jerry Farley ◽  
Heather A. Drummond
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Underlying Mechanism ◽  
Bk Channels ◽  
Bk Channel ◽  
Vitro Assay ◽  
Whole Cell ◽  
Residual Currents ◽  
Renal Vascular

Myogenic constrictor responses in small renal arteries and afferent arterioles are suppressed in mice with reduced levels of β-epithelial Na+ channel (βENaCm/m). The underlying mechanism is unclear. Decreased activity of voltage-gated calcium channels (VGCC) or mechanically gated ion channels and increased activity of large conductance calcium-activated potassium (BK) channels are a few possible mechanisms. The purpose of this study was to determine if VGCC, BK, or mechanically gated ion channel activity was altered in renal vascular smooth muscle cell (VSMC) from βENaCm/m mice. To address this, we used whole cell patch-clamp electrophysiological approaches in freshly isolated renal VSMCs. Compared with βENaC+/+ controls, the current-voltage relationships for VGCC and BK activity are similar in βENaCm/m mice. These findings suggest neither VGCC nor BK channel dysfunction accounts for reduced myogenic constriction in βENaCm/m mice. We then examined mechanically gated currents using a novel in vitro assay where VSMCs are mechanically activated by stretching an underlying elastomer. We found the mechanically gated currents, predominantly carried by Na+, are observed with less frequency (87 vs. 43%) and have smaller magnitude (−54.1 ± 12.5 vs. −20.9 ± 4.9 pA) in renal VSMCs from βENaCm/m mice. Residual currents are expected in this model since VSMC βENaC expression is reduced by 50%. These findings suggest βENaC is required for normal mechanically gated currents in renal VSMCs and their disruption may account for the reduced myogenic constriction in the βENaCm/m model. Our findings are consistent with the role of βENaC as a VSMC mechanosensor and function of evolutionarily related nematode degenerin proteins.

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