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Artykuły w czasopismach na temat „BKCa channels”

Autor: Grafiati

Data publikacji: 7 grudnia 2024

Data aktualizacji: 31 lipca 2025

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1

Zhu, Shu, Darren D. Browning, Richard E. White, David Fulton та Scott A. Barman. "Mutation of protein kinase C phosphorylation site S1076 on α-subunits affects BKCa channel activity in HEK-293 cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 297, № 4 (2009): L758—L766. http://dx.doi.org/10.1152/ajplung.90518.2008.

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Large conductance, calcium- and voltage-activated potassium (BKCa) channels are important modulators of pulmonary vascular smooth muscle membrane potential, and phosphorylation of BKCa channels by protein kinases regulates pulmonary arterial smooth muscle function. However, little is known about the effect of phosphorylating specific channel subunits on BKCa channel activity. The present study was done to determine the effect of mutating protein kinase C (PKC) phosphorylation site serine 1076 (S1076) on transfected human BKCa channel α-subunits in human embryonic kidney (HEK-293) cells, a hete

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2

Zhao, Guiling, Zachary P. Neeb, M. Dennis Leo, et al. "Type 1 IP3 receptors activate BKCa channels via local molecular coupling in arterial smooth muscle cells." Journal of General Physiology 136, no. 3 (2010): 283–91. http://dx.doi.org/10.1085/jgp.201010453.

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Plasma membrane large-conductance Ca2+-activated K+ (BKCa) channels and sarcoplasmic reticulum inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are expressed in a wide variety of cell types, including arterial smooth muscle cells. Here, we studied BKCa channel regulation by IP3 and IP3Rs in rat and mouse cerebral artery smooth muscle cells. IP3 activated BKCa channels both in intact cells and in excised inside-out membrane patches. IP3 caused concentration-dependent BKCa channel activation with an apparent dissociation constant (Kd) of ∼4 µM at physiological voltage (−40 mV) and intracellu

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3

Xie, Man-Jiang, Yu-Guang Ma, Fang Gao, et al. "Activation of BKCa channel is associated with increased apoptosis of cerebrovascular smooth muscle cells in simulated microgravity rats." American Journal of Physiology-Cell Physiology 298, no. 6 (2010): C1489—C1500. http://dx.doi.org/10.1152/ajpcell.00474.2009.

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Cerebral arterial remodeling is one of the critical factors in the occurrence of postspaceflight orthostatic intolerance. We hypothesize that large-conductance calcium-activated K+ (BKCa) channels in vascular smooth muscle cells (VSMCs) may play an important role in regulating cerebrovascular adaptation during microgravity exposure. The aim of this work was to investigate whether activation of BKCa channels is involved in regulation of apoptotic remodeling of cerebral arteries in simulated microgravity rats. In animal studies, Sprague-Dawley rats were subjected to 1-wk hindlimb unweighting to

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4

Ling, Shizhang, Jian-Zhong Sheng, and Andrew P. Braun. "The calcium-dependent activity of large-conductance, calcium-activated K+ channels is enhanced by Pyk2- and Hck-induced tyrosine phosphorylation." American Journal of Physiology-Cell Physiology 287, no. 3 (2004): C698—C706. http://dx.doi.org/10.1152/ajpcell.00030.2004.

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Recent results showing that large-conductance, calcium-activated K+ (BKCa) channels undergo direct tyrosine phosphorylation in the presence of c-Src tyrosine kinase have suggested the involvement of these channels in Src-mediated signaling pathways. Given the important role for c-Src in integrin-mediated signal transduction, we have examined the potential regulation of BKCa channels by proline-rich tyrosine kinase 2 (Pyk2), a calcium-sensitive tyrosine kinase activated upon integrin stimulation. Transient coexpression of murine BKCa channels with either wild-type Pyk2 or hematopoietic cell kin

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5

Kim, Eun Young, Jae Mi Suh, Yu-Hsin Chiu, and Stuart E. Dryer. "Regulation of podocyte BKCa channels by synaptopodin, Rho, and actin microfilaments." American Journal of Physiology-Renal Physiology 299, no. 3 (2010): F594—F604. http://dx.doi.org/10.1152/ajprenal.00206.2010.

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Mechanosensitive large-conductance Ca2+-activated K+ channels encoded by the Slo1 gene (BKCa channels) are expressed in podocytes. Here we show that BKCa channels reciprocally coimmunoprecipitate with synaptopodin (Synpo) in mouse glomeruli, in mouse podocytes, and in a heterologous expression system (HEK293T cells) in which these proteins are transiently expressed. Synpo and Slo1 colocalize along the surface of the glomerular basement membrane in mouse glomeruli. Synpo interacts with BKCa channels at COOH-terminal domains that overlap with an actin-binding domain on the channel molecule that

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6

Werner, Matthias E., Andrea L. Meredith, Richard W. Aldrich, and Mark T. Nelson. "Hypercontractility and impaired sildenafil relaxations in the BKCa channel deletion model of erectile dysfunction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 1 (2008): R181—R188. http://dx.doi.org/10.1152/ajpregu.00173.2008.

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Erectile dysfunction (ED) can be elicited by a variety of pathogenic factors, particularly impaired formation of and responsiveness to nitric oxide (NO) and the downstream effectors soluble guanylate cyclase (sGC) and cGMP-dependent protein kinase I (PKGI). One important target of PKGI in smooth muscle is the large-conductance, Ca2+-activated potassium (BKCa) channel. In our previous report ( 42 ), we demonstrated that deletion of the BKCa channel in mice induced force oscillations and led to reduced nerve-evoked relaxations and ED. In the current study, we used this ED model to explore the ro

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7

Choi, Chang-Rok, Eun-Jin Kim, Tae Hyun Choi, Jaehee Han, and Dawon Kang. "Enhancing Human Cutaneous Wound Healing through Targeted Suppression of Large Conductance Ca2+-Activated K+ Channels." International Journal of Molecular Sciences 25, no. 2 (2024): 803. http://dx.doi.org/10.3390/ijms25020803.

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The modulation of K+ channels plays a crucial role in cell migration and proliferation, but the effect of K+ channels on human cutaneous wound healing (CWH) remains underexplored. This study aimed to determine the necessity of modulating K+ channel activity and expression for human CWH. The use of 25 mM KCl as a K+ channel blocker markedly improved wound healing in vitro (in keratinocytes and fibroblasts) and in vivo (in rat and porcine models). K+ channel blockers, such as quinine and tetraethylammonium, aided in vitro wound healing, while Ba2+ was the exception and did not show similar effec

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8

Barman, Scott A., Shu Zhu, and Richard E. White. "Protein kinase C inhibits BKCa channel activity in pulmonary arterial smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 1 (2004): L149—L155. http://dx.doi.org/10.1152/ajplung.00207.2003.

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Signaling mechanisms that elevate cyclic AMP (cAMP) activate large-conductance, calcium- and voltage-activated potassium (BKCa) channels in pulmonary vascular smooth muscle and cause pulmonary vasodilatation. BKCa channel modulation is important in the regulation of pulmonary arterial pressure, and inhibition (closing) of the BKCa channel has been implicated in the development of pulmonary vasoconstriction. Protein kinase C (PKC) causes pulmonary vasoconstriction, but little is known about the effect of PKC on BKCa channel activity. Accordingly, studies were done to determine the effect of PKC

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9

Khan, Raheela N., Stephen K. Smith, J. J. Morrison, and Michael L. J. Ashford. "Ca2+ dependence and pharmacology of large-conductance K+ channels in nonlabor and labor human uterine myocytes." American Journal of Physiology-Cell Physiology 273, no. 5 (1997): C1721—C1731. http://dx.doi.org/10.1152/ajpcell.1997.273.5.c1721.

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Two populations, Ca2+-dependent (BKCa) and Ca2+-independent K+ (BK) channels of large conductance were identified in inside-out patches of nonlabor and labor freshly dispersed human pregnant myometrial cells, respectively. Cell-attached recordings from nonlabor myometrial cells frequently displayed BKCa channel openings characterized by a relatively low open-state probability, whereas similar recordings from labor tissue displayed either no channel openings or consistently high levels of channel activity that often exhibited clear, oscillatory activity. In inside-out patch recordings, Ba2+ (2–

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10

Hou, Shangwei, Stefan H. Heinemann, and Toshinori Hoshi. "Modulation of BKCa Channel Gating by Endogenous Signaling Molecules." Physiology 24, no. 1 (2009): 26–35. http://dx.doi.org/10.1152/physiol.00032.2008.

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Large-conductance Ca2+- and voltage-activated K+ (BKCa, MaxiK, or Slo1) channels are expressed in almost every tissue in our body and participate in many critical functions such as neuronal excitability, vascular tone regulation, and neurotransmitter release. The functional versatility of BKCa channels owes in part to the availability of a spectacularly wide array of biological modulators of the channel function. In this review, we focus on modulation of BKCa channels by small endogenous molecules, emphasizing their molecular mechanisms. The mechanistic information available from studies on th

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11

Hannigan, K. I., R. J. Large, E. Bradley, et al. "Effect of a novel BKCa opener on BKCa currents and contractility of the rabbit corpus cavernosum." American Journal of Physiology-Cell Physiology 310, no. 4 (2016): C284—C292. http://dx.doi.org/10.1152/ajpcell.00273.2015.

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Large-conductance Ca2+-activated K+ (BKCa) channels are thought to play a key role in the regulation of corpus cavernosum smooth muscle (CCSM) excitability. Few BKCa channel openers have been accepted for clinical development. The effect of the novel BKCa channel opener GoSlo-SR5-130 on electrical activity in isolated rabbit CCSM cells and mechanical activity in strips of rabbit CCSM was examined. Single-channel currents were observed in inside-out patches. These channels were sensitive to Ca2+, blocked by penitrem A, and had a conductance of 291 ± 20 pS ( n = 7). In the presence of GoSlo-SR5-

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12

Chang, Wei-Ting, and Sheng-Nan Wu. "Effective Activation of BKCa Channels by QO-40 (5-(Chloromethyl)-3-(Naphthalen-1-yl)-2-(Trifluoromethyl)Pyrazolo [1,5-a]pyrimidin-7(4H)-one), Known to Be an Opener of KCNQ2/Q3 Channels." Pharmaceuticals 14, no. 5 (2021): 388. http://dx.doi.org/10.3390/ph14050388.

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QO-40 (5-(chloromethyl)-3-(naphthalene-1-yl)-2-(trifluoromethyl) pyrazolo[1,5-a]pyrimidin-7(4H)-one) is a novel and selective activator of KCNQ2/KCNQ3 K+ channels. However, it remains largely unknown whether this compound can modify any other type of plasmalemmal ionic channel. The effects of QO-40 on ion channels in pituitary GH3 lactotrophs were investigated in this study. QO-40 stimulated Ca2+-activated K+ current (IK(Ca)) with an EC50 value of 2.3 μM in these cells. QO-40-stimulated IK(Ca) was attenuated by the further addition of GAL-021 or paxilline but not by linopirdine or TRAM-34. In

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13

Niloy, Sayeman Islam, Yue Shen, Lirong Guo, Stephen T. O’Rourke, and Chengwen Sun. "Loss of IP3R-BKCa Coupling Is Involved in Vascular Remodeling in Spontaneously Hypertensive Rats." International Journal of Molecular Sciences 24, no. 13 (2023): 10903. http://dx.doi.org/10.3390/ijms241310903.

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Mechanisms by which BKCa (large-conductance calcium-sensitive potassium) channels are involved in vascular remodeling in hypertension are not fully understood. Vascular smooth muscle cell (VSMC) proliferation and vascular morphology were compared between hypertensive and normotensive rats. BKCa channel activity, protein expression, and interaction with IP3R (inositol 1,4,5-trisphosphate receptor) were examined using patch clamp, Western blot analysis, and coimmunoprecipitation. On inside-out patches of VSMCs, the Ca2+-sensitivity and voltage-dependence of BKCa channels were similar between hyp

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14

Sansom, Steven C., Rong Ma, Pamela K. Carmines, and David A. Hall. "Regulation of Ca2+-activated K+ channels by multifunctional Ca2+/calmodulin-dependent protein kinase." American Journal of Physiology-Renal Physiology 279, no. 2 (2000): F283—F288. http://dx.doi.org/10.1152/ajprenal.2000.279.2.f283.

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Activation of mesangial cells by ANG II provokes release of intracellular Ca2+ stores and subsequent Ca2+influx through voltage-gated channels, events that are reflected by a large transient increase in intracellular concentration [Ca2+]i followed by a modest sustained elevation in [Ca2+]i. These ANG II-induced alterations in [Ca2+]i elicit activation of large Ca2+-activated K+ channels (BKCa) in a negative-feedback manner. The mechanism of this BKCa feedback response may involve the direct effect of intracellular Ca2+ on the channel and/or channel activation by regulatory enzymes. The present

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15

Yokoshiki, Hisashi, Takashi Seki, Masanori Sunagawa, and Nicholas Sperelakis. "Inhibition of Ca2+-activated K+ channels by tyrosine phosphatase inhibitors in rat mesenteric artery." Canadian Journal of Physiology and Pharmacology 78, no. 9 (2000): 745–50. http://dx.doi.org/10.1139/y00-042.

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To investigate the possible regulation of large-conductance Ca2+-activated K+ channels (BKCa) by tyrosine phosphatases (Tyr-PPs), single-channel currents of myocytes from rat mesenteric artery were recorded in open cell-attached patches. Two structurally different Tyr-PP inhibitors, sodium orthovanadate (Na3VO4) and dephostatin, were used. The channels (236 pS) evoked at +40 mV and pCa 6, were significantly inhibited by 1 mM Na3VO4 (-81 ± 3%, n = 10; P < 0.005). Similarly, 100 µM dephostatin strongly inhibited the BKCa channels (-80 ± 7%, n = 7 ; P < 0.05). Therefore, BKCa channels in va

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16

Paisansathan, Chanannait, Haoliang Xu, Francesco Vetri, Moises Hernandez, and Dale A. Pelligrino. "Interactions between adenosine and K+ channel-related pathways in the coupling of somatosensory activation and pial arteriolar dilation." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 6 (2010): H2009—H2017. http://dx.doi.org/10.1152/ajpheart.00702.2010.

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Multiple, perhaps interactive, mechanisms participate in the linkage between increased neural activity and cerebral vasodilation. In the present study, we assessed whether neural activation-related pial arteriolar dilation (PAD) involved interactions among adenosine (Ado) A2 receptors (A2Rs), large-conductance Ca2+-operated K+ (BKCa) channels, and inward rectifier K+ (Kir) channels. In rats with closed cranial windows, we monitored sciatic nerve stimulation (SNS)-induced PAD in the absence or presence of pharmacological blockade of A2Rs (ZM-241385), ecto-5′-nucleotidase (α,β-methylene-adenosin

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17

Lu, Te-Ling, Zi-Han Gao, Shih-Wei Li, and Sheng-Nan Wu. "High Efficacy by GAL-021: A Known Intravenous Peripheral Chemoreceptor Modulator that Suppresses BKCa-Channel Activity and Inhibits IK(M) or Ih." Biomolecules 10, no. 2 (2020): 188. http://dx.doi.org/10.3390/biom10020188.

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GAL-021 has recently been developed as a novel breathing control modulator. However, modifications of ionic currents produced by this agent remain uncertain, although its efficacy in suppressing the activity of big-conductance Ca2+-activated K+ (BKCa) channels has been reported. In pituitary tumor (GH3) cells, we found that the presence of GAL-021 decreased the amplitude of macroscopic Ca2+-activated K+ current (IK(Ca)) in a concentration-dependent manner with an effective IC50 of 2.33 μM. GAL-021-mediated reduction of IK(Ca) was reversed by subsequent application of verteporfin or ionomycin;

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18

Riddle, Melissa A., Jennifer M. Hughes, and Benjimen R. Walker. "Role of caveolin-1 in endothelial BKCa channel regulation of vasoreactivity." American Journal of Physiology-Cell Physiology 301, no. 6 (2011): C1404—C1414. http://dx.doi.org/10.1152/ajpcell.00013.2011.

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A novel vasodilatory influence of endothelial cell (EC) large-conductance Ca2+-activated K+ (BKCa) channels is present following in vivo exposure to chronic hypoxia (CH) and may exist in other pathological states. However, the mechanism of channel activation that results in altered vasoreactivity is unknown. We tested the hypothesis that CH removes an inhibitory effect of the scaffolding domain of caveolin-1 (Cav-1) on EC BKCa channels to permit activation, thereby affecting vasoreactivity. Experiments were performed on gracilis resistance arteries and ECs from control and CH-exposed (380 mmHg

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19

Barman, Scott A., Shu Zhu, and Richard E. White. "PKC activates BKCa channels in rat pulmonary arterial smooth muscle via cGMP-dependent protein kinase." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 6 (2004): L1275—L1281. http://dx.doi.org/10.1152/ajplung.00259.2003.

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Normally, signaling mechanisms that activate large-conductance, calcium- and voltage-activated potassium (BKCa) channels in pulmonary vascular smooth muscle cause pulmonary vasodilatation. BKCa-channel modulation is important in the regulation of pulmonary arterial pressure, and inhibition (decrease in the opening probability) of the BKCa channel has been implicated in the development of pulmonary vasoconstriction. Protein kinase C (PKC) causes pulmonary vasoconstriction, but little is known about the effect of PKC on BKCa-channel activity in pulmonary vascular smooth muscle. Accordingly, stud

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20

Mizutani, Hiroya, Hisao Yamamura, Makoto Muramatsu, Yumiko Hagihara, Yoshiaki Suzuki, and Yuji Imaizumi. "Modulation of Ca2+ oscillation and melatonin secretion by BKCa channel activity in rat pinealocytes." American Journal of Physiology-Cell Physiology 310, no. 9 (2016): C740—C747. http://dx.doi.org/10.1152/ajpcell.00342.2015.

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The pineal glands regulate circadian rhythm through the synthesis and secretion of melatonin. The stimulation of nicotinic acetylcholine receptor due to parasympathetic nerve activity causes an increase in intracellular Ca2+ concentration and eventually downregulates melatonin production. Our previous report shows that rat pinealocytes have spontaneous and nicotine-induced Ca2+ oscillations that are evoked by membrane depolarization followed by Ca2+ influx through voltage-dependent Ca2+ channels (VDCCs). These Ca2+ oscillations are supposed to contribute to the inhibitory mechanism of melatoni

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21

Szteyn, Kalina, and Harpreet Singh. "BKCa Channels as Targets for Cardioprotection." Antioxidants 9, no. 8 (2020): 760. http://dx.doi.org/10.3390/antiox9080760.

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The large-conductance calcium- and voltage-activated K+ channel (BKCa) are encoded by the Kcnma1 gene. They are ubiquitously expressed in neuronal, smooth muscle, astrocytes, and neuroendocrine cells where they are known to play an important role in physiological and pathological processes. They are usually localized to the plasma membrane of the majority of the cells with an exception of adult cardiomyocytes, where BKCa is known to localize to mitochondria. BKCa channels couple calcium and voltage responses in the cell, which places them as unique targets for a rapid physiological response. T

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22

Gururaja Rao, Shubha, Piotr Bednarczyk, Atif Towheed, et al. "BKCa (Slo) Channel Regulates Mitochondrial Function and Lifespan in Drosophila melanogaster." Cells 8, no. 9 (2019): 945. http://dx.doi.org/10.3390/cells8090945.

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BKCa channels, originally discovered in Drosophila melanogaster as slowpoke (slo), are recognized for their roles in cellular and organ physiology. Pharmacological approaches implicated BKCa channels in cellular and organ protection possibly for their ability to modulate mitochondrial function. However, the direct role of BKCa channels in regulating mitochondrial structure and function is not deciphered. Here, we demonstrate that BKCa channels are present in fly mitochondria, and slo mutants show structural and functional defects in mitochondria. slo mutants display an increase in reactive oxy

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23

Li, N., R. Shi, Y. Ye, et al. "Aging-induced down-regulation of Pka/Bkca pathway in rat cerebral arteries." Physiological Research 71, no. 6 (2022): 811–23. http://dx.doi.org/10.33549/physiolres.934944.

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The incidence of cerebrovascular diseases increases significantly with aging. This study aimed to test the hypothesis that aging may influence the protein kinase A (PKA)-dependent vasodilation via RyR/BKCa pathway in the middle cerebral arteries (MCA). Male Sprague-Dawley rats were randomly divided into control (4-6 month-old) and aged (24-month-old) groups. The functions of MCA and ion channel activities in smooth muscle cells were examined using myograph system and patch-clamp. Aging decreased the isoproterenol/forskolin-induced relaxation in the MCA. Large-conductance Ca2+-activated-K+ (BKC

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Herrera, Gerald M., Thomas J. Heppner, and Mark T. Nelson. "Voltage dependence of the coupling of Ca2+ sparks to BKCa channels in urinary bladder smooth muscle." American Journal of Physiology-Cell Physiology 280, no. 3 (2001): C481—C490. http://dx.doi.org/10.1152/ajpcell.2001.280.3.c481.

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Large-conductance Ca2+-dependent K+(BKCa) channels play a critical role in regulating urinary bladder smooth muscle (UBSM) excitability and contractility. Measurements of BKCa currents and intracellular Ca2+ revealed that BKCa currents are activated by Ca2+ release events (Ca2+ sparks) from ryanodine receptors (RyRs) in the sarcoplasmic reticulum. The goals of this project were to characterize Ca2+ sparks and BKCa currents and to determine the voltage dependence of the coupling of RyRs (Ca2+ sparks) to BKCachannels in UBSM. Ca2+ sparks in UBSM had properties similar to those described in arter

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Idres, Sarah, Germain Perrin, Valérie Domergue, et al. "Contribution of BKCa channels to vascular tone regulation by PDE3 and PDE4 is lost in heart failure." Cardiovascular Research 115, no. 1 (2018): 130–44. http://dx.doi.org/10.1093/cvr/cvy161.

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Abstract Aims Regulation of vascular tone by 3′,5′-cyclic adenosine monophosphate (cAMP) involves many effectors including the large conductance, Ca2+-activated, K+ (BKCa) channels. In arteries, cAMP is mainly hydrolyzed by type 3 and 4 phosphodiesterases (PDE3, PDE4). Here, we examined the specific contribution of BKCa channels to tone regulation by these PDEs in rat coronary arteries, and how this is altered in heart failure (HF). Methods and results Concomitant application of PDE3 (cilostamide) and PDE4 (Ro-20-1724) inhibitors increased BKCa unitary channel activity in isolated myocytes fro

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Dimitropoulou, Christiana, Guichun Han, Allison W. Miller, et al. "Potassium (BKCa) currents are reduced in microvascular smooth muscle cells from insulin-resistant rats." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 3 (2002): H908—H917. http://dx.doi.org/10.1152/ajpheart.00382.2001.

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Insulin resistance (IR) syndrome is associated with impaired vascular relaxation; however, the underlying pathophysiology is unknown. Potassium channel activation causes vascular smooth muscle hyperpolarization and relaxation. The present study determined whether a reduction in large conductance calcium- and voltage-activated potassium (BKCa) channel activity contributes to impaired vascular relaxation in IR rats. BKCa channels were characterized in mesenteric microvessels from IR and control rats. Macroscopic current density was reduced in myocytes from IR animals compared with controls. In a

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27

Darkow, D. J., L. Lu, and R. E. White. "Estrogen relaxation of coronary artery smooth muscle is mediated by nitric oxide and cGMP." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (1997): H2765—H2773. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2765.

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Estrogens are proposed to exert protection against cardiovascular disease, and evidence now suggests that this protection involves a direct vasodilatory effect. We have shown previously that estrogen relaxes endothelium-denuded porcine coronary arteries by opening the large-conductance calcium- and voltage-activated potassium (BKCa) channel of myocytes through guanosine 3',5'-cyclic monophosphate (cGMP)-dependent phosphorylation (35). The present study confirms these results and now demonstrates that this mechanism involves production of nitric oxide (NO). S-nitroso-N-acetylpenicillamine (SNAP

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Chen, Yin-Chia, Chia-Lung Shih, Chao-Liang Wu, Yi-Hsien Fang, Edmund Cheung So, and Sheng-Nan Wu. "Exploring the Impact of BKCa Channel Function in Cellular Membranes on Cardiac Electrical Activity." International Journal of Molecular Sciences 25, no. 3 (2024): 1537. http://dx.doi.org/10.3390/ijms25031537.

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This review paper delves into the current body of evidence, offering a thorough analysis of the impact of large-conductance Ca2+-activated K+ (BKCa or BK) channels on the electrical dynamics of the heart. Alterations in the activity of BKCa channels, responsible for the generation of the overall magnitude of Ca2+-activated K+ current at the whole-cell level, occur through allosteric mechanisms. The collaborative interplay between membrane depolarization and heightened intracellular Ca2+ ion concentrations collectively contribute to the activation of BKCa channels. Although fully developed mamm

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Guntur, Divya, Horst Olschewski, Péter Enyedi, Réka Csáki, Andrea Olschewski, and Chandran Nagaraj. "Revisiting the Large-Conductance Calcium-Activated Potassium (BKCa) Channels in the Pulmonary Circulation." Biomolecules 11, no. 11 (2021): 1629. http://dx.doi.org/10.3390/biom11111629.

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Potassium ion concentrations, controlled by ion pumps and potassium channels, predominantly govern a cell′s membrane potential and the tone in the vessels. Calcium-activated potassium channels respond to two different stimuli-changes in voltage and/or changes in intracellular free calcium. Large conductance calcium-activated potassium (BKCa) channels assemble from pore forming and various modulatory and auxiliary subunits. They are of vital significance due to their very high unitary conductance and hence their ability to rapidly cause extreme changes in the membrane potential. The pathophysio

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Li, Yan, Jin Bai, Yi-hua Yang, Naoto Hoshi, and Dong-bao Chen. "Hydrogen Sulfide Relaxes Human Uterine Artery via Activating Smooth Muscle BKCa Channels." Antioxidants 9, no. 11 (2020): 1127. http://dx.doi.org/10.3390/antiox9111127.

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Opening of large conductance calcium-activated and voltage-dependent potassium (BKCa) channels hyperpolarizes plasma membranes of smooth muscle (SM) to cause vasodilation, underling a key mechanism for mediating uterine artery (UA) dilation in pregnancy. Hydrogen sulfide (H2S) has been recently identified as a new UA vasodilator, yet the mechanism underlying H2S-induced UA dilation is unknown. Here, we tested whether H2S activated BKCa channels in human UA smooth muscle cells (hUASMC) to mediate UA relaxation. Multiple BKCa subunits were found in human UA in vitro and hUASMC in vitro, and high

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Wang, Wei, Haixia Huang, Dongyan Hou, et al. "Mechanosensitivity of STREX-lacking BKCa channels in the colonic smooth muscle of the mouse." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 6 (2010): G1231—G1240. http://dx.doi.org/10.1152/ajpgi.00268.2010.

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Stretch sensitivity of Ca2+-activated large-conductance K+ channels (BKCa) has been observed in a variety of cell types and considered to be a potential mechanism in mechanoelectric transduction (MET). Mechanical stress is a major stimulator for the smooth muscle in the gastrointestinal (GI) tract. However, much about the role and mechanism of MET in GI smooth muscles remains unknown. The BKCa shows a functional diversity due to intensive Slo I alternative splicing and different α/β-subunit assembly in various cells. The stress-regulated exon (STREX) insert is suggested to be an indispensable

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Shieh, D. B., S. R. Yang, X. Y. Shi, Y. N. Wu, and S. N. Wu. "Properties of BKCa Channels in Oral Keratinocytes." Journal of Dental Research 84, no. 5 (2005): 468–73. http://dx.doi.org/10.1177/154405910508400513.

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Keratinocytes are important for epithelial antimicrobial barrier function. The activity of ion channels can affect the proliferation of keratinocytes. Little is known about Ca2+-activated K+ currents in these cells. Ion currents in normal human oral keratinocytes were characterized with a patch-clamp technique. In whole-cell configuration, depolarizing pulses evoked K+ outward currents ( IK) in oral keratinocytes. Iberiotoxin (200 nM) and paxilline (1 μM) suppressed IK; however, neither apamin (200 nM) nor 5-hydroxydecanoate (30 μM) had any effects on it. Caffeic acid phenethyl ester, a compou

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Braun, Andrew P. "Ammonium ion enhances the calcium-dependent gating of a mammalian large conductance, calcium-sensitive K+ channel." Canadian Journal of Physiology and Pharmacology 79, no. 11 (2001): 919–23. http://dx.doi.org/10.1139/y01-076.

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We observed that the current amplitude and activation of expressed, mouse brain large conductance, calcium-sensitive K+ channels (BKCa channels) may be reversibly enhanced following addition of low concentrations of the weakly permeant cation NH4+ to the cytoplasmic face of the channel in excised, inside-out membrane patches from HEK 293 cells. Conductance-voltage relations were left-shifted along the voltage axis by addition of NH4Cl in a concentration-dependent manner, with an EC50 of 18.5 mM. Furthermore, this effect was observed in the presence of cytosolic free calcium (~1 µM), but was ab

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Bao, Lin, та Daniel H. Cox. "Gating and Ionic Currents Reveal How the BKCa Channel's Ca2+ Sensitivity Is Enhanced by its β1 Subunit". Journal of General Physiology 126, № 4 (2005): 393–412. http://dx.doi.org/10.1085/jgp.200509346.

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Large-conductance Ca2+-activated K+ channels (BKCa channels) are regulated by the tissue-specific expression of auxiliary β subunits. β1 is predominately expressed in smooth muscle, where it greatly enhances the BKCa channel's Ca2+ sensitivity, an effect that is required for proper regulation of smooth muscle tone. Here, using gating current recordings, macroscopic ionic current recordings, and unitary ionic current recordings at very low open probabilities, we have investigated the mechanism that underlies this effect. Our results may be summarized as follows. The β1 subunit has little or no

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Lynch, Fiona M., Sarah B. Withers, Zhihong Yao, et al. "Perivascular adipose tissue-derived adiponectin activates BKCa channels to induce anticontractile responses." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 6 (2013): H786—H795. http://dx.doi.org/10.1152/ajpheart.00697.2012.

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This study aims to identify the potential mechanisms by which perivascular adipose tissue (PVAT) reduces tone in small arteries. Small mesenteric arteries from wild-type and large-conductance Ca2+-activated K+ (BKCa) channel knockout mice were mounted on a wire myograph in the presence and absence of PVAT, and contractile responses to norepinephrine were assessed. Electrophysiology studies were performed in isolated vessels to measure changes in membrane potential produced by adiponectin. Contractile responses from wild-type mouse small arteries were significantly reduced in the presence of PV

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Hannah, Rachael M., Kathryn M. Dunn, Adrian D. Bonev, and Mark T. Nelson. "Endothelial SKCa and IKCa Channels Regulate Brain Parenchymal Arteriolar Diameter and Cortical Cerebral Blood Flow." Journal of Cerebral Blood Flow & Metabolism 31, no. 5 (2010): 1175–86. http://dx.doi.org/10.1038/jcbfm.2010.214.

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Calcium-sensitive potassium (KCa) channels have been shown to modulate the diameter of cerebral pial arteries; however, little is known regarding their roles in controlling cerebral parenchymal arterioles (PAs). We explored the function and cellular distribution of small-conductance (SKCa) and intermediate-conductance (IKCa) KCa channels and large-conductance KCa (BKCa) channels in endothelial cells (ECs) and smooth muscle cells (SMCs) of PAs. Both SKCa and IKCa channels conducted the outward current in isolated PA ECs (current densities, ~20 pA/pF and ~28 pA/pF at + 40 mV, respectively), but

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Qian, Lingling, Xiaoyu Liu, and Ruxing Wang. "Role of BKCa channels in diabetic vascular complications." Chinese Medical Journal 127, no. 9 (2014): 1775–81. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20132503.

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Objective This review focuses on the role of the large conductance calcium-activated potassium (BKCa) channels in diabetic vascular complications. Data sources Relevant articles published in English or Chinese from 1981 to present were selected from PubMed. The search terms were “BKCa channels” and “diabetes”. Important references from selected articles were also retrieved. Study selection Articles regarding the role of BKCa channels in diabetic vascular complications and relevant mechanisms were selected. Results The BKCa channels are abundantly expressed in vascular smooth cells and play an

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Fallet, Rachel W., Joseph P. Bast, Keiji Fujiwara, Naohito Ishii, Steven C. Sansom, and Pamela K. Carmines. "Influence of Ca2+-activated K+ channels on rat renal arteriolar responses to depolarizing agonists." American Journal of Physiology-Renal Physiology 280, no. 4 (2001): F583—F591. http://dx.doi.org/10.1152/ajprenal.2001.280.4.f583.

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Experiments were performed to evaluate the hypothesis that opening of Ca2+-activated K+ channels (BKCachannels) promotes juxtamedullary arteriolar dilation and curtails constrictor responses to depolarizing agonists. Under baseline conditions, afferent and efferent arteriolar lumen diameters averaged 23.4 ± 0.9 ( n = 36) and 22.8 ± 1.1 ( n= 13) μm, respectively. The synthetic BKCa channel opener NS-1619 evoked concentration-dependent afferent arteriolar dilation. BKCa channel blockade (1 mM tetraethylammonium; TEA) decreased afferent diameter by 15 ± 3% and prevented the dilator response to 30

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Campbell, William B., Blythe B. Holmes, John R. Falck, Jorge H. Capdevila, and Kathryn M. Gauthier. "Regulation of potassium channels in coronary smooth muscle by adenoviral expression of cytochrome P-450 epoxygenase." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 1 (2006): H64—H71. http://dx.doi.org/10.1152/ajpheart.00516.2005.

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Epoxyeicosatrienoic acids (EETs) are endothelium-derived cytochrome P-450 (CYP) metabolites of arachidonic acid that relax vascular smooth muscle by large-conductance calcium-activated potassium (BKCa) channel activation and membrane hyperpolarization. We hypothesized that if smooth muscle cells (SMCs) had the capacity to synthesize EETs, endogenous EET production would increase BKCa channel activity. Bovine coronary SMCs were transduced with adenovirus coding the CYP Bacillus megaterium -3 (F87V) (CYP BM-3) epoxygenase that metabolizes arachidonic acid exclusively to 14( S),15( R)-EET. Adenov

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Kang, Lori S., SeJeong Kim, James M. Dominguez, Amy L. Sindler, Gregory M. Dick, and Judy M. Muller-Delp. "Aging and muscle fiber type alter K+ channel contributions to the myogenic response in skeletal muscle arterioles." Journal of Applied Physiology 107, no. 2 (2009): 389–98. http://dx.doi.org/10.1152/japplphysiol.91245.2008.

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Aging diminishes myogenic tone in arterioles from skeletal muscle. Recent evidence indicates that both large-conductance Ca2+-activated (BKCa) and voltage-dependent (KV) K+ channels mediate negative feedback control of the myogenic response. Thus we tested the hypothesis that aging increases the contributions of KV and BKCa channels to myogenic regulation of vascular tone. Because myogenic responsiveness differs between oxidative and glycolytic muscles, we predicted that KV and BKCa channel contributions to myogenic responsiveness vary with fiber type. Myogenic responses of first-order arterio

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Sweet, Tara-Beth, та Daniel H. Cox. "Measuring the Influence of the BKCa β1 Subunit on Ca2+ Binding to the BKCa Channel". Journal of General Physiology 133, № 2 (2009): 139–50. http://dx.doi.org/10.1085/jgp.200810129.

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The large-conductance Ca2+-activated potassium (BKCa) channel of smooth muscle is unusually sensitive to Ca2+ as compared with the BKCa channels of brain and skeletal muscle. This is due to the tissue-specific expression of the BKCa auxiliary subunit β1, whose presence dramatically increases both the potency and efficacy of Ca2+ in promoting channel opening. β1 contains no Ca2+ binding sites of its own, and thus the mechanism by which it increases the BKCa channel's Ca2+ sensitivity has been of some interest. Previously, we demonstrated that β1 stabilizes voltage sensor activation, such that a

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Cordeiro, Brenda, Dmitry Terentyev, and Richard T. Clements. "BKCa channel activation increases cardiac contractile recovery following hypothermic ischemia/reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 4 (2015): H625—H633. http://dx.doi.org/10.1152/ajpheart.00818.2014.

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Mitochondrial Ca2+-activated large-conductance K+ (BKCa) channels are thought to provide protection during ischemic insults in the heart. Rottlerin (mallotoxin) has been implicated as a potent BKCa activator. The purpose of this study was twofold: 1) to investigate the efficacy of BKCa channel activation as a cardioprotective strategy during ischemic cardioplegic arrest and reperfusion (CP/R) and 2) to assess the specificity of rottlerin for BKCa channels. Wild-type (WT) and BKCa knockout (KO) mice were subjected to an isolated heart model of ischemic CP/R. A mechanism of rottlerin-induced car

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Rosenfeld, Charles R., David N. Cornfield та Timothy Roy. "Ca2+-activated K+ channels modulate basal and E2β-induced rises in uterine blood flow in ovine pregnancy". American Journal of Physiology-Heart and Circulatory Physiology 281, № 1 (2001): H422—H431. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h422.

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Uterine blood flow (UBF) increases >30-fold during ovine pregnancy. During the last trimester, this reflects vasodilation, which may be due to placentally derived estrogens. In nonpregnant ewes, estradiol-17β (E2β) increases UBF >10-fold by activating nitric oxide synthase and large conductance calcium-dependent potassium channels (BKCa). To determine whether BKCa channels modulate basal and E2β-induced increases in UBF, studies were performed in near-term pregnant ewes with uterine artery flow probes and catheters for intra-arterial infusions of tetraethylammonium (TEA), a selective BKC

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Savalli, Nicoletta, Andrei Kondratiev, Sarah Buxton de Quintana, Ligia Toro та Riccardo Olcese. "Modes of Operation of the BKCa Channel β2 Subunit". Journal of General Physiology 130, № 1 (2007): 117–31. http://dx.doi.org/10.1085/jgp.200709803.

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The β2 subunit of the large conductance Ca2+- and voltage-activated K+ channel (BKCa) modulates a number of channel functions, such as the apparent Ca2+/voltage sensitivity, pharmacological and kinetic properties of the channel. In addition, the N terminus of the β2 subunit acts as an inactivating particle that produces a relatively fast inactivation of the ionic conductance. Applying voltage clamp fluorometry to fluorescently labeled human BKCa channels (hSlo), we have investigated the mechanisms of operation of the β2 subunit. We found that the leftward shift on the voltage axis of channel a

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Borbouse, Léna, Gregory M. Dick, Shinichi Asano, et al. "Impaired function of coronary BKCa channels in metabolic syndrome." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (2009): H1629—H1637. http://dx.doi.org/10.1152/ajpheart.00466.2009.

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The role of large-conductance Ca2+-activated K+ (BKCa) channels in regulation of coronary microvascular function is widely appreciated, but molecular and functional changes underlying the deleterious influence of metabolic syndrome (MetS) have not been determined. Male Ossabaw miniature swine consumed for 3–6 mo a normal diet (11% kcal from fat) or an excess-calorie atherogenic diet that induces MetS (45% kcal from fat, 2% cholesterol, 20% kcal from fructose). MetS significantly impaired coronary vasodilation to the BKCa opener NS-1619 in vivo (30–100 μg) and reduced the contribution of these

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Bai, Bing, Nanjuan Lu, Wei Zhang, et al. "Inhibitory Effects of Genistein on Vascular Smooth Muscle Cell Proliferation Induced by Ox-LDL: Role of BKCa Channels." Analytical Cellular Pathology 2020 (December 13, 2020): 1–12. http://dx.doi.org/10.1155/2020/8895449.

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Background. Oxidized low-density lipoprotein (Ox-LDL) is a crucial pathogenic factor for vascular diseases, which can induce the proliferation of vascular smooth muscle cells (VSMCs). Genistein is the main component of soybean isoflavone. Genistein has a variety of pharmacological properties in the treatment of vascular diseases and a promising clinical application. Large-conductance calcium-activated potassium (BKCa) channels are the primary type of potassium channels in VSMCs, which regulate various biological functions of VSMCs. However, whether genistein exerts an antiproliferation effect

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Zhao, T., H. Zhang, C. Jin, F. Qiu, Y. Wu, and L. Shi. "Melatonin mediates vasodilation through both direct and indirect activation of BKCa channels." Journal of Molecular Endocrinology 59, no. 3 (2017): 219–33. http://dx.doi.org/10.1530/jme-17-0028.

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Melatonin, synthesized primarily by the pineal gland, is a neuroendocrine hormone with high membrane permeability. The vascular effects of melatonin, including vasoconstriction and vasodilation, have been demonstrated in numerous studies. However, the mechanisms underlying these effects are not fully understood. Large-conductance Ca2+-activated K+ (BKCa) channels are expressed broadly on smooth muscle cells and play an important role in vascular tone regulation. This study explored the mechanisms of myocyte BKCa channels and endothelial factors underlying the action of melatonin on the mesente

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Storer, RJ, DC Immke, R. Yin, and PJ Goadsby. "Large Conductance Calcium-Activated Potassium Channels (BKCa) Modulate Trigeminovascular Nociceptive Transmission." Cephalalgia 29, no. 12 (2009): 1242–58. http://dx.doi.org/10.1111/j.1468-2982.2009.01849.x.

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Migraine is a common, disabling, neurological problem whose acute management would benefit from the development of purely neurally acting therapies. The trigeminocervical complex is pivotal in nociceptive signaling in migraine, and is an accepted target for putative antimigraine agents. Whole-cell patch-clamp or extracellular recordings were made of trigeminal neurons identified in rat brainstem slices. Bath application of the large conductance calcium-activated potassium (BKCa) channel opener NS1619 caused a dramatic decrease of cell firing that could be reversed by the co-application of iber

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Kim, Eun Young, Shengwei Zou, Lon D. Ridgway та Stuart E. Dryer. "β1-Subunits Increase Surface Expression of a Large-Conductance Ca2+-Activated K+ Channel Isoform". Journal of Neurophysiology 97, № 5 (2007): 3508–16. http://dx.doi.org/10.1152/jn.00009.2007.

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Auxiliary (beta) subunits of large-conductance Ca2+-activated K+ (BKCa) channels regulate the gating properties of the functional channel complex. Here we show that an avian β1-subunit also stimulates the trafficking of BKCa channels to the plasma membrane in HEK293T cells and in a native population of developing vertebrate neurons. One C-terminal variant of BKCa α-subunits, called the VEDEC isoform after its five last residues, is largely retained in intracellular compartments when it is heterologously expressed in HEK293T cells. A closely related splice variant, called QEERL, shows high leve

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Zhang, Q., Y. Bai, Z. Yang, J. Tian, and Z. Meng. "The molecular mechanism of the effect of sulfur dioxide inhalation on the potassium and calcium ion channels in rat aortas." Human & Experimental Toxicology 35, no. 4 (2015): 418–27. http://dx.doi.org/10.1177/0960327115591375.

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This study investigated the molecular mechanism of the effect of sulfur dioxide (SO2) on the expression of adenosine triphosphate (ATP)-sensitive potassium ion (K+; KATP) channel, big-conductance calcium ion (Ca2+)-activated K+ (BKCa) channel, and L-type (L-Ca2+) channel subunits in rat aortas with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot. The results showed that the messenger RNA and protein levels of the KATP channel subunits Kir6.1, Kir6.2, and sulfonylurea receptor 2B (SUR2B) of rat aortas were significantly increased by SO2 at 14 mg/m3, where

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