Potassium channels in airway smooth muscle: A tale of two channels
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Regulation of Ca<sup>2 +</sup>-Sensitive K<sup>+</sup> Channels by Cholesterol and Bile Acids via Distinct Channel Subunits and Sites
2017, Current Topics in MembranesCitation Excerpt :In spite of these generalizations, functional diversity and distinct regulatory roles of BK channels in specific CNS regions and peripheral tissues arise from different current phenotypes due to differential BK subunit expression, β subunits in particular (Lorenz, Heils, Kasper, & Sander, 2007; Orio et al., 2002; Pape, Munsch, & Budde, 2004; Shao, Halvorsrud, Borg-Graham, & Storm, 1999; Wang, Ding, Xia, & Lingle, 2002; Xia, Ding, & Lingle, 1999). Other processes in which BK play a fundamental role are regulation of neurotransmitter and hormone release (Yazejian, Sun, & Grinnell, 2000), suppression of high-frequency cycles in the auditory system (Fettiplace & Fuchs, 1999; Ramanathan & Fuchs, 2002), relaxation of vascular (Brayden & Nelson, 1992; Brenner, Jegla, Wickenden, Liu, & Aldrich, 2000; Jaggar, Porter, Lederer, & Nelson, 2000), and nonvascular smooth muscle (Choudhury, Garg, Singh, & Mishra, 2011; France, Bhattarai, Galligan, & Xu, 2012; Heppner, Herrera, Bonev, Hill-Eubanks, & Nelson, 2003; Kotlikoff, 1993; Semenov, Wang, Herlihy, & Brenner, 2006), flow-induced K+ secretion in the nephron distal segment (Grimm, Foutz, Brenner, & Sansom, 2007), K+ secretion in the distal colon (Sausbier et al., 2006), and cancer proliferation and metastasis (Bloch et al., 2007; Khaitan et al., 2009; Sontheimer, 2008). Manipulation of CLR content at the organ level can be achieved by a high CLR diet which effectively evokes hypercholesterolemia in animal models, including rat and mouse (reviewed by Bukiya & Rosnehouse-Dantsker, 2015).
Novel treatment strategies for smooth muscle disorders: Targeting Kv7 potassium channels
2016, Pharmacology and TherapeuticsCitation Excerpt :Membrane voltage is largely determined by potassium (K+) channel activity, and hence, K+ channels are often central mediators in the physiological modulation of smooth muscle contractility. Multiple types of K+ channels are expressed in smooth muscle cells; several excellent review articles have been written describing their contribution to the regulation of smooth muscle cell contractility (Kotlikoff, 1993; Nelson and Quayle, 1995; Vogalis, 2000; Khan et al., 2001; Brainard et al., 2007; Greenwood & Ohya, 2009; Petkov, 2011; Jepps et al., 2013; Greenwood and Tribe, 2014; Stott et al., 2014). This review will focus on Kv7 (KCNQ) K+ channels, a specific subtype of K+ channels recently recognized for its important contributions to the regulation of smooth muscle cell contractility in viscera, vasculature, and airways.
Vasorelaxant activity of 7-β-O-glycosides biosynthesized from flavonoids
2014, European Journal of PharmacologyCitation Excerpt :The glycosylated derivative (3) begins to appear in the reaction medium from 24 h after the addition, reaching a maximum concentration in 48 h and then decreasing until 96 h. (2), disappeared from the reaction medium at 24 h and has the highest concentration of derivative (4) in 96 h. Naringenin-7-O-glycoside (3) is also found in plants (prunin) (Desiderio et al., 2005; Vitor et al., 2004) and has shown similar pharmaceutical profile when compared to the aglycones (Choi et al., 1991; Kotlikoff 1993; Manthey and Guthrie, 2002). Its synthesis has been reported, to our knowledge, only using Sophora flavescens to produce 4, 7-di-β-O-glucoside, which was hydrolyzed to obtain 7-β-O-glycoside in very low yield (1.9%) (Yamamoto et al., 2004).
Large conductance, calcium- and voltage-gated potassium (BK) channels: Regulation by cholesterol
2012, Pharmacology and TherapeuticsCitation Excerpt :In vascular smooth muscle, BK channel opening leads to spontaneous transient outward currents (STOCs) that tend to hyperpolarize the cell membrane and, thus, oppose depolarization-induced smooth muscle contraction (Brayden & Nelson, 1992; Brenner et al., 2000b; Jaggar et al., 2000; Pérez et al., 2001). Likewise, Ca2+-spark regulation of STOCs plays a physiological role in controlling the myogenic tone in the urinary bladder (Heppner et al., 2003), and BK channels play a critical role in regulating airway smooth muscle tone (Kotlikoff, 1993; Semenov et al., 2006). Vascular myocyte BK channels are additionally targeted by endothelial factors that regulate vasomotion, such as nitric oxide (NO), prostaglandin I2, and epoxyeicosatrienoic acid (Tanaka et al., 2004; Félétou & Vanhoutte, 2006).
Ion channels in asthma
2011, Journal of Biological ChemistryCitation Excerpt :Potassium channels contribute to the relaxation of ASM by hyperpolarizing the membrane potential and thereby preventing the activation of VGCCs. Electrophysiological and molecular approaches have facilitated the identification of several K+ channels in ASM (although for some, only indirect evidence exists): Ca2+-activated K+ channels (KCa), voltage-activated K+ channels (Kv), and ATP-sensitive K+ channels (KATP) (65–68). Despite their clear contribution to ASM physiology, evidence for their involvement in asthma pathophysiology is scant.
Ion channel regulation of intracellular calcium and airway smooth muscle function
2009, Pulmonary Pharmacology and TherapeuticsCitation Excerpt :KCa channels also differ in their sensitivity to inhibitors allowing their different actions to be assessed pharmacologically; KCa1.1 channels are inhibited by TEA, iberiotoxin and charybdotoxin whereas KCa3.1 channels are inhibited by TRAM-34, clotrimazole, ICA17043 and charybdotoxin [120,122]. A Ca2+-dependent and voltage-gated outward K+ current that is sensitive to charybdotoxin and iberiotoxin is widely found in isolated tracheal SMCs [123–125]. The properties of this current are consistent with the large conductance KCa channel (BK or KCa1.1); a channel commonly responsible for spontaneous transient outward currents (STOCS) that are associated with ‘Ca2+ sparks’ [126].